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Bibliography on: Mitochondrial Evolution

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Robert J. Robbins is a biologist, an educator, a science administrator, a publisher, an information technologist, and an IT leader and manager who specializes in advancing biomedical knowledge and supporting education through the application of information technology. More About:  RJR | OUR TEAM | OUR SERVICES | THIS WEBSITE

RJR: Recommended Bibliography 10 Mar 2026 at 02:00 Created: 

Mitochondrial Evolution

The endosymbiotic hypothesis for the origin of mitochondria (and chloroplasts) suggests that mitochondria are descended from specialized bacteria (probably purple nonsulfur bacteria) that somehow survived endocytosis by another species of prokaryote or some other cell type, and became incorporated into the cytoplasm.

Created with PubMed® Query: ( mitochondria AND evolution NOT 26799652[PMID] NOT 33634751[PMID] NOT 38225003[PMID]) NOT pmcbook NOT ispreviousversion

Citations The Papers (from PubMed®)

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RevDate: 2026-03-09

Žihala D, Salamonová J, M Eliáš (2026)

Corrigendum to "Evolution of the genetic code in the mitochondria of Labyrinthulea (Stramenopiles)" [Mol. Phylogenet. Evol. 152 (2020) 106908].

RevDate: 2026-03-09
CmpDate: 2026-03-09

Schoenle A, Francis O, Archibald JM, et al (2025)

Protist genomics: key to understanding eukaryotic evolution.

Trends in genetics : TIG, 41(10):868-882.

All eukaryotes other than animals, plants, and fungi are protists. Protists are highly diverse and found in nearly all environments, with key roles in planetary health and biogeochemical cycles. They represent the majority of eukaryotic diversity, making them essential for understanding eukaryotic evolution. However, these mainly unicellular, microscopic organisms are understudied and the generation of protist genomes lags far behind most multicellular lineages. Current genomic methods, which are primarily designed for animals and plants, are poorly suited for protists. Advancing protist genome research requires reevaluating plant- and animal-centric genomic standards. Future efforts must leverage emerging technologies and bioinformatics tools, ultimately enhancing our understanding of eukaryotic molecular and cell biology, ecology, and evolution.

RevDate: 2026-03-08
CmpDate: 2026-03-08

Bhalodi JA, Surm JM, AM Reitzel (2026)

Transcription dynamics and regulation of heat shock protein genes during stress and development in the estuarine cnidarian Nematostella vectensis.

Comparative biochemistry and physiology. Part D, Genomics & proteomics, 58:101754.

Heat shock proteins (HSPs) are molecular chaperones that function in protecting cells from proteotoxicity. Eukaryotes have multiple HSPs that localize in the cytoplasm, endoplasmic reticulum (ER), and mitochondria. In cnidarian species, where HSPs are often used as biomarkers of environmental stress, little is known about how particular HSPs vary in copy number, expression, inducibility, and regulation within a species. Here, we characterized the full repertoire of HSP70 and HSP90 genes in an emerging model cnidarian, Nematostella vectensis. We identified five HSP70 and three HSP90 genes, with at least one homolog from each family belonging to the three primary clades based on subcellular localization. Although transcriptional induction remained insignificant by a 10 °C temperature change, two cytosolic HSP70s and one cytosolic HSP90 were significantly upregulated with a 20 °C temperature increase. Most HSPs exhibited similar developmental expression patterns, with elevated expression during the early larval stage followed by reduced expression in the juvenile stage. HSPs showed evidence for differential expression across cell types, with multiple cytosolic and ER HSPs being highly expressed in neuronal and cnidocyte populations. Moreover, the putative promoters of N. vectensis HSPs differed in both the abundance and sequences of regulatory heat shock element motifs, providing a potential mechanism of functional diversification in response to temperature and development. By characterizing expression of all HSP70 and HSP90 genes in this cnidarian, we reveal distinct roles of these core chaperones in the proteostasis response, providing a foundation for future functional studies on contributions of HSPs to cnidarian life cycle and stress resilience.

RevDate: 2026-03-07

Martin WF (2026)

Demand-only energetics at 120 ATP per glucose: A reply to Lynch.

Biochimica et biophysica acta. Bioenergetics, 1867(2):149587 pii:S0005-2728(26)00007-1 [Epub ahead of print].

Recently in these pages, a paper by Lynch appeared in response to a report showing that his numbers for biosynthetic costs (ATP demand) in cells are inflated, so much so that they would require E. coli to obtain >100 ATP per glucose and mitochondria to obtain >240 ATP per glucose. The inflated estimates trace to one factor: Lynch exclusively considers ATP demand and systematically neglects ATP supply-the essence of bioenergetics. Thermodynamics stipulate that a cell cannot grow if its ATP demands exceed its ATP supply. Here I compare Lynch's calculated ATP demands to laboratory measurements of the ATP supply that E. coli synthesizes during cell division. The results bear out my case, and leave no doubt: Lynch's calculations require E. coli to synthesize ∼120 ATP per glucose, which is thermodynamically impossible. As a consequence, his demand-only 'energetic' attacks on mitochondria and endosymbiosis in evolution are baseless.

RevDate: 2026-03-07
CmpDate: 2026-03-07

Khan A, Ziyi Y, Rahman FU, et al (2026)

The Impact of Mitochondrial DNA Depletion on Mitochondrial Ultrastructure, Photosynthesis, and the mTERF Gene Family in Chlamydomonas reinhardtii.

International journal of molecular sciences, 27(4):.

Mitochondrial biogenesis requires coordinated expression from both nuclear and mitochondrial genomes. To understand the consequences of mitochondrial genome loss, we generated a mitochondrial DNA-depleted line (crm[-]) in Chlamydomonas reinhardtii via long-term ethidium bromide treatment. We then examined how mtDNA disruption affects mitochondrial ultrastructure, chloroplast function, and the mitochondrial transcription termination factor (mTERF) gene family. Our results reveal that mitochondrial dysfunction is associated with severe organelle remodeling, including mitochondrial elongation, matrix condensation, and cristae collapse. Consequently, mitochondria reduce the electron sink capacity which appears to over-reduce the chloroplast electron transport chain, correlating with causing damage to photosystem II (PSII), as indicated by higher plastoquinone PQ redox state and PSII excitation pressure and lower non-photochemical quantum yield [Y(NPQ)]. Furthermore, we identified and characterized eight nuclear-encoded mTERF genes in C. reinhardtii (CrmTERFs). Phylogenetic analysis grouped them into three clades with potential functional conservation. Collinearity analysis suggested potential evolutionary relationships between mTERF genes in Chlamydomonas and Marchantia polymorpha. Gene ontology annotation linked CrmTERFs to transcription termination and RNA biosynthesis regulation. Additionally, in silico prediction identified twelve putative miRNAs targeting seven of the eight CrmTERFs, with CrmTERF3 as the only exception, providing candidates for future experimental validation. This study provides the first comprehensive analysis of the nuclear encoded mTERF gene family in Chlamydomonas and demonstrates that mtDNA loss is correlated with mTERF genes expression, as well as mitochondrial structure and chloroplast photoprotective impairments. These findings suggest a potential role for CrmTERFs in mitochondrial retrograde signaling and organellar crosstalk, though functional validation is required to establish causality.

RevDate: 2026-03-07
CmpDate: 2026-03-07

Wang L, Li H, Shi Y, et al (2026)

Functional characterization of the Rab11 and its response to SGIV infection in the orange-spotted grouper (Epinephelus coioides).

Fish & shellfish immunology, 172:111230.

Rab11, a member of the Rab GTPase family, serves as a key regulator of vesicular trafficking and modulates viral infection in mammals, yet its functional role in aquatic viral infection remains largely uncharacterized. Singapore grouper iridovirus (SGIV), a member of the genus Ranavirus in the family Iridoviridae, is one of the most important viral pathogens afflicting grouper aquaculture. In this study, we investigated the influence of a novel Rab11 homolog (EcRab11) from the orange-spotted grouper (Epinephelus coioides) on SGIV infection and the role in host innate immune responses. EcRab11 shares high amino acid sequence identity with Rab11 orthologs spanning from mammals to teleost fishes, indicating evolutionary conservation of this GTPase. In healthy groupers, EcRab11 was predominantly expressed in major immune organs including the liver and spleen, and its transcript levels were significantly upregulated following immune challenges. Confocal imaging revealed that EcRab11 localizes to the cytoplasm as distinct punctate and vesicle-like structures. In contrast, overexpression of a constitutively active EcRab11 mutant (CA-EcRab11, with a GTP-locked mutation at the conserved Q70L site that renders the protein persistently activated and unable to hydrolyze GTP to GDP) induced the formation of enlarged vesicular structures, whereas overexpression of a dominant-negative EcRab11 mutant (DN-EcRab11, with a GDP-locked mutation at the conserved S25N site that abrogates GTP binding and locks the protein in an inactive state) resulted in a marked reduction in vesicle formation. Co-localization analyses further demonstrated that EcRab11 extensively colocalizes with the Golgi apparatus, early endosomes and late endosomes, and partially with the endoplasmic reticulum or lysosomes, but did not colocalize with mitochondria. Functional assays revealed that EcRab11 overexpression significantly suppressed SGIV infection, whereas overexpression of either CA-EcRab11 or DN-EcRab11 enhanced viral replication. Moreover, EcRab11 was found to positively regulate both autophagy and IFN immune responses in grouper cells. Taken together, our findings demonstrate that EcRab11 modulates SGIV infection by orchestrating host innate immune responses, thereby uncovering a novel antiviral mechanism of Rab11 against SGIV and providing new insights for the development of antiviral strategies for grouper aquaculture.

RevDate: 2026-03-07
CmpDate: 2026-03-07

Fan Y, Wang N, Wang S, et al (2026)

GhGLDH35A gene-mediated ROS homeostasis and stomatal movement via the ascorbic acid pathway confers alkaline stress tolerance.

Journal of advanced research, 81:75-94.

INTRODUCTION: Ascorbic acid (AsA) is involved in plant responses to various abiotic stresses. However, its specific function in alkaline stress tolerance remains poorly understood. The L-galactono-1,4-lactone dehydrogenase (GLDH) gene is crucial for AsA synthesis, yet the precise role of GLDH in modulating plant resistance to alkaline stress has not been comprehensively characterized.

OBJECTIVES: To investigate the role of GLDH genes in enhancing tolerance to alkaline stress.

METHODS: Bioinformatics analysis of the GLDH gene family members was conducted, and an evolutionary tree was constructed using MEGA software. Cis-acting elements and gene structures were analyzed using TBtools. Gene expression levels were quantified by qRT-PCR, while the function of the GhGLDH35A gene was validated through VIGS (Virus-induced gene silencing) in cotton, heterologous overexpression in Arabidopsis thaliana, and complementation assays in yeast.

RESULTS: Our study investigated the effects of salt-alkaline stress on cotton and found that alkaline stress caused significantly more severe damage than salt stress. The GLDH family genes were identified and analyzed, revealing a high degree of evolutionary conservation. Most GhGLDH genes exhibited a positive response to alkaline stress and were regulated by light. Among them, GhGLDH35A, which is highly expressed within the GLDH family, was found to play a key role in conferring tolerance to alkaline stress. Subcellular localization analysis indicated that GhGLDH35A is localized in the mitochondria. Silencing of GhGLDH35A in cotton resulted in reduced tolerance to alkaline stress, disruption of ROS homeostasis, and impairment of photosynthesis and stomatal function. Conversely, overexpression of GhGLDH35A in Arabidopsis enhanced alkaline stress resistance by elevating AsA levels, increasing antioxidant enzyme activities to enhance ROS scavenging, sustaining photosynthesis, and promoting stomatal closure. Furthermore, heterologous expression of GhGLDH35A in yeast also improved its tolerance to alkaline stress.

CONCLUSIONS: GhGLDH35A positively regulates alkaline stress tolerance by enhancing antioxidant defenses and regulating stomatal movement.

RevDate: 2026-03-06
CmpDate: 2026-03-06

Tan J, Zeng Y, Zhu H, et al (2026)

Berberine Attenuates Intracranial Aneurysm Formation by Activating SIRT1 to Suppress HMGB1 Acetylation and NF-κB Signaling.

Neurochemical research, 51(2):.

The formation of intracranial aneurysms (IAs) is linked to metabolic problems and functional abnormalities in vascular smooth muscle cells (VSMCs). Berberine (BBR), a tetracyclic alkaloid having anti-inflammatory, antioxidant, and energy metabolism regulatory capabilities, has an unknown impact in IA progression. The purpose of this study is to look at the effects of BBR on IA development and the molecular mechanisms that drive it. An elastase-induced rat IA model was established as previously described, with in vivo measurements of aneurysm incidence, rupture rates, and artery structural integrity. An in vitro damage model was created by using primary VSMCs treated with Ang II. Inflammatory reactions, oxidative stress, mitochondrial function, and energy metabolism were investigated. The SIRT1/HMGB1/NF-κB signaling axis was investigated by Western blotting, immunofluorescence, pharmacological inhibition (EX-527), genetic manipulation (SIRT1 overexpression or HMGB1 knockdown/overexpression), and mitochondrial-targeted therapies (Antimycin A, MitoTEMPO). BBR dramatically reduced IA development and rupture in rats, reducing arterial inflammation and structural damage. In vitro, BBR restored Ang II-induced VSMC dysfunction, including mitochondrial depolarization, ROS overproduction, glycolytic shift, and inflammation, by upregulating SIRT1, increasing its binding to HMGB1, and decreasing HMGB1 acetylation, cytoplasmic translocation, and NF-κB activity. EX-527 eliminated these benefits, whereas SIRT1 overexpression replicated them, revealing SIRT1's important involvement. Loss- and gain-of-function studies revealed that HMGB1 operates downstream of SIRT1, and that mitochondrial integrity is critical: Antimycin A inhibited BBR's actions, but MitoTEMPO mimicked them. BBR promotes SIRT1 to deacetylate HMGB1, preventing its cytoplasmic translocation and NF-κB-mediated inflammation. Importantly, mitochondrial dysfunction caused by Ang II or IA disease is a primary driver of metabolic dysregulation and inflammatory activation in VSMCs. By maintaining mitochondrial integrity, BBR restores bioenergetic and redox equilibrium, breaking the inflammatory-metabolic vicious cycle. These coordinated responses inhibit the formation and evolution of cerebral aneurysms.

RevDate: 2026-03-06
CmpDate: 2026-03-06

Gusmão IV, Figueredo RTA, Corrêa LL, et al (2026)

Integrative taxonomy reveals a novel Ceratomyxa (Cnidaria: Myxozoa) parasitizing the gallbladder of the Amazonian fish Pellona castelnaeana.

Acta tropica, 275:108005.

Freshwater species of the myxozoan genus Ceratomyxa have recently emerged as a diverse group of parasites infecting fish in South America, many of which exhibit vermiform plasmodia with dynamic motility. In this integrative taxonomic study, we describe Ceratomyxa souzapintorum n. sp., a novel species infecting the gallbladder of the Amazonian clupeiform fish Pellona castelnaeana. The prevalence of infection was 73%, and the parasite displayed worm-like plasmodia exhibiting nematode-like motility. Arcuate myxospores measured 14.8 ± 1.7 µm in thickness and 6.1 ± 0.7 µm in length, with a posterior angle of 59° (42-78°). The two spherical nematocysts measured 2.0 µm and contained filaments with 3-4 coils. Ultrastructural analyses revealed plasmodia consisting of an outer cytoplasmic region containing sporogonic stages and numerous tubular mitochondria, and internally a large central vacuole. Mature plasmodia exhibited a thin cytoplasmic layer, with mature myxospores apparently free within the central vacuole. Phylogenetic analyses positioned C. souzapintorum n. sp. within the clade of Amazonian Ceratomyxa species.

RevDate: 2026-03-06
CmpDate: 2026-03-06

Gudiksen A, Hansen CC, van der Stede T, et al (2026)

MOTS-c improves intrinsic muscle mitochondrial bioenergetic health and efficiency in a PGC-1α/AMPK-dependent manner.

Free radical biology & medicine, 246:682-696.

Mitochondrial-derived peptides are a small class of regulatory peptides encoded by short open reading frames in mitochondrial DNA. One such peptide, mitochondrial open reading frame of the 12S rRNA-c (MOTS-c), has been shown to exert numerous beneficial effects on whole-cell and systemic metabolic parameters when administered exogenously. However, potential MOTS-c-mediated effects on mitochondrial bioenergetics have been largely overlooked. Therefore, the primary aim of the present study was to elucidate whether and, if so, how MOTS-c regulates skeletal muscle (SkM) mitochondrial function. We demonstrate, using two distinct transgenic mouse strains, that administration of MOTS-c augments muscle mitochondrial bioenergetic performance through reliance on both the transcriptional coactivator, Peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), and cellular energy-sensing kinase, 5' adenosine monophosphate-activated protein kinase (AMPK). These effects seem to be exerted without apparent impact on mitochondrial respiratory protein content, alluding to intrinsic mitochondrial changes rather than changes in volume. Furthermore, MOTS-c treatment lowers mitochondrial reactive oxygen species (ROS) emission and ROS-related protein damage indicating substantial alleviation of cellular oxidative stress. RNA-sequence data reveal the effects of MOTS-c treatment to potentially be exerted subtly across a number of mitochondrial parameters such as redox handling, mitochondrial integrity and OXPHOS efficiency, jointly indicating a mechanistic basis for the observed functional improvements in mitochondrial bioenergetics. Despite increased interstitial MOTS-c levels no change was observed in the arterio-venous difference during one-legged knee extensor exercise in humans. This suggests that SkM may not be the source of circulating MOTS-c in response to exercise.

RevDate: 2026-03-05
CmpDate: 2026-03-05

Lisa AK, Reeve WG, Laird DW, et al (2026)

The complete mitochondrial genome of Dunaliella salina CS-265: insights into gene content and phylogenetic placement.

Mitochondrial DNA. Part B, Resources, 11(4):468-472 pii:2635789.

We report the complete mitochondrial genome of the halotolerant green alga Dunaliella salina CS-265, isolated from a hypersaline lake in central Australia. The genome is a circular DNA molecule of 30,073 bp, encoding seven protein-coding genes, nine rRNAs, and three tRNAs. Four core genes (cox1, cob, nad1, and nad5) are fragmented by multiple introns, whereas others remain intact. The absence of ATP synthase subunits and ribosomal protein genes reflects ongoing reductive evolution in Dunaliella mitochondria. This genome adds a new organellar resource from an Australian isolate, complementing previous studies and providing further insight into mitochondrial genome dynamics in halotolerant green algae.

RevDate: 2026-03-04

Huang C, Wang B, Yu J, et al (2026)

Convergent evolutionary shifts in AGT targeting between mitochondria and peroxisomes across mammal transitions to herbivory.

Nature communications, 17(1):.

Herbivory has evolved multiple times during mammalian diversification, playing a key role in the success of this globally distributed clade. A central metabolic challenge for herbivores is the detoxification of glyoxylate. The enzyme alanine:glyoxylate aminotransferase (AGT) converts glyoxylate to glycine, preventing the formation of harmful calcium oxalate crystals. AGT localizes to mitochondria and peroxisomes based on the mitochondrial targeting sequence (MTS) and the peroxisomal targeting signal (PTS1), respectively. While most studies focused on MTS, MTS variation alone does not fully explain AGT localization patterns. To assess the relative importance of the PTS1 motif, we combined comparative sequence analyses with functional assays. We find that multiple herbivorous lineages underwent independent mutations resulting in disrupted or truncated MTS regions, whereas the PTS1 motif remains functional. Immunofluorescence assays revealed more efficient peroxisomal localization of AGT in herbivores, with PTS1 often overriding mitochondrial signals even when the MTS is intact. Additionally, transcriptomic analyses show that several herbivorous lineages preferentially use downstream transcriptional start sites, producing AGT isoforms lacking the MTS. Together, our findings reveal a central role of AGT peroxisomal targeting in evolution of plant-based diets, and demonstrate how increased targeting efficiency has evolved convergently via the interplay of transcriptional regulation and targeting signals.

RevDate: 2026-03-02

Lai KL, Smith TB, Maroofian R, et al (2026)

Expanding the genotypic spectrum of combined oxidative phosphorylation deficiency 54.

Neurogenetics, 27(1):.

RevDate: 2026-03-01

Zeller LM, Schorn S, Nicolas-Asselineau L, et al (2026)

Redox gradients define the ecological niche of ciliates with denitrifying endosymbionts in anoxic lake waters.

The ISME journal pii:8502596 [Epub ahead of print].

Bacterial endosymbionts of the family Ca. Azoamicaceae obligately associate with anaerobic ciliates belonging to the class Plagiopylea. The symbionts' unique role for their host involves anaerobic respiration of nitrate and generation of ATP, analogous to the role of mitochondria in aerobic eukaryotes. As this symbiosis remains so far uncultured, insights into its functioning have been mainly inferred from environmental metagenomes. Here we investigated the distribution and environmental role of this symbiosis in the anoxic basins of two freshwater lakes Zug and Lugano (Switzerland) over a course of several years. We found that the environmental niche of the ciliate host is defined by the combined effects of sulfide, oxygen and nitrate, the latter of which is essential for the symbiont's respiratory function. Moreover, the distribution and abundances of ciliates with denitrifying endosymbionts in the water column suggests that they may substantially contribute to nitrate consumption in Lake Zug. Our microscopic analyses further demonstrated a coordinated division of the Candidatus Azoamicus ciliaticola symbionts and their ciliate hosts, implying a vertical inheritance of denitrifying symbionts. These observations offer new insights into the evolution of ciliates with denitrifying endosymbionts and their ecological role in oxygen-depleted lakewaters.

RevDate: 2026-02-27

Marton J, Ciocan RA, Bâldea I, et al (2026)

Molecular Mechanisms, Dynamic Lesions, and Therapeutic Targets in Intestinal Ischemia-Reperfusion Injury: A Systematic Review.

International journal of molecular sciences, 27(4): pii:ijms27041763.

Intestinal ischemia-reperfusion injury (IRI) represents a major cause of morbidity and mortality in abdominal surgery, trauma, and intestinal transplantation. The pathophysiological process involves a biphasic cascade that begins with ischemic hypoxia and progresses to amplified cellular and molecular injury upon reperfusion. This review synthesizes recent mechanistic insights regarding endothelial and microvascular dysfunction, epithelial barrier breakdown, microbiota-driven systemic propagation, and the involvement of oxidative/nitrosative stress and inflammatory signaling. The novelty of our review's approach is the focus on experimental and translational studies and correlation of the data with future directions for mechanistic research and clinical implementation. Despite promising preclinical results, heterogeneity in study protocols or/and model limitations make clinical translation challenging. Recent studies have demonstrated that mitochondria, tight junction proteins, adhesion molecules and innate immune receptors are critical determinants of lesion evolution. Based on these, the current therapeutic strategies include antioxidants, adenosine pathway modulators, dexmedetomidine, ischemic conditioning, hyperbaric oxygen therapy, and microbiota-targeted interventions. Since each mechanism is acting on distinct molecular pathways, a multimodal therapy that integrates redox modulation, endothelial protection, microbiome regulation, and the identification and employment of precision biomarkers is likely to improve outcomes. Beyond summarizing established molecular mechanisms, this review critically reassesses why decades of promising experimental strategies for intestinal ischemia-reperfusion injury has largely failed to translate into effective clinical therapies. By distinguishing context-dependent mechanisms from pathways with consistent translational relevance, we highlight key methodological and biological barriers limiting clinical applicability. Furthermore, we propose a temporally structured, multimodal therapeutic framework that integrates phase-specific pathophysiology with targeted interventions, aiming to inform future experimental design and improve translational success.

RevDate: 2026-02-25

Huang Y, He T, Zheng J, et al (2026)

Circular RNAs in metabolic health: bridging the gap between molecular biology and therapy.

Cell death & disease pii:10.1038/s41419-026-08450-5 [Epub ahead of print].

Recent advances in obesity research have shifted focus toward biological mechanisms, paralleling progress in pharmacotherapy. Fat browning-the conversion of white to brown adipocytes-emerges as a promising therapeutic strategy. Circular RNAs (circRNAs), stable non-coding RNAs with regulatory functions, are now recognized as key modulators of this process through organelle-mediated mechanisms. This review synthesizes current understanding of circRNA biogenesis and their roles in fat browning, particularly their interactions with mitochondria and endoplasmic reticulum in lipid metabolism. We highlight their capacity to encode peptides and regulate metabolic pathways, positioning circRNAs as potential precision therapeutics. While preclinical studies demonstrate mechanistic efficacy, clinical translation requires addressing delivery challenges and tissue-specific effects. This biological perspective advances obesity treatment paradigms beyond simplistic energy-balance models, mirroring the evolution seen in pharmacotherapeutic development.

RevDate: 2026-02-23

Pang J, Zhang Y, Tian Y, et al (2026)

Mapping the scientific landscape of mitochondria-associated membranes: a bibliometric insight into emerging frontiers in aging and diseases.

International journal of surgery (London, England) pii:01279778-990000000-04688 [Epub ahead of print].

BACKGROUND: Mitochondria-associated membranes (MAMs) are critical hubs coordinating energy metabolism, lipid homeostasis, and Ca2[+] signaling, thereby regulating cell survival, stress responses, and apoptosis. Increasing evidence links MAMs dysfunction to aging, neurodegenerative diseases, metabolic disorders, and cancer. Although numerous mechanistic studies and narrative reviews have been published, a systematic, mechanism-oriented bibliometric evaluation of the global MAMs research landscape is still lacking.

METHODS: We performed a comprehensive bibliometric analysis of MAMs-related literature indexed in the Web of Science Core Collection from 2009 to 2024, using Bibliometrix, VOSviewer, and CiteSpace to integrate publication trends, collaboration networks, keyword co-occurrence, thematic evolution, and citation impact.

RESULTS: A total of 1199 publications were identified, showing a rapid annual growth rate of 21.57%. Beyond general trend analysis, our study reveals that research hotspots converge on Ca2⁺ homeostasis, ER stress, apoptosis, and mitochondrial dynamics, and progressively shift toward aging-related biological processes. By mapping high-frequency keywords to known MAMs-associated pathways, we identify aging, ER stress, and apoptosis as interconnected emerging themes. Importantly, this analysis highlights specific MAMs-related proteins, including HSP90α, as potential regulatory hubs linking stress responses and aging.

CONCLUSIONS: This study provides the first integrative, mechanism-oriented bibliometric framework of MAMs research, bridging quantitative publication patterns with underlying biological pathways. Our findings not only delineate the intellectual structure and evolving themes of the field but also generate testable hypotheses implicating MAMs and key regulatory proteins in aging-related processes, thereby offering guidance for future mechanistic and translational studies.

RevDate: 2026-02-20
CmpDate: 2026-02-20

Unten Y, Takafuji K, Masukagami Y, et al (2026)

Characterizing mitochondrial phenotypes and MERCS in aged human skeletal muscle myoblasts.

PloS one, 21(2):e0343604 pii:PONE-D-25-62412.

Age-associated declines in skeletal muscle function are linked to cellular senescence and mitochondrial alterations, yet mitochondrial phenotypes in aged human myoblasts remain insufficiently characterized. Here, we examined primary skeletal muscle myoblasts from young and elderly donors to assess mitochondrial function, morphology, and mitochondria-endoplasmic reticulum (ER) contact sites (MERCS). Myoblasts from older donors exhibited senescence features, including elevated SA-β-gal activity and reduced Lamin B1 expression, accompanied by increased mitochondrial oxidative stress. Despite marked mitochondrial hyperfusion and increased mitochondrial DNA content, mitochondrial oxygen consumption rate and membrane potential per mitochondrial area were comparable between young and old cells. MERCS were significantly elevated in aged myoblasts and were reduced by scavenging mitochondrial reactive oxygen species (mtROS), indicating an association between oxidative stress and MERCS formation. These findings suggest that mitochondrial hyperfusion and enhanced MERCS accompany cellular aging in human myoblasts and may contribute to maintaining mitochondrial function under elevated oxidative stress.

RevDate: 2026-02-20
CmpDate: 2026-02-20

Meduri GU, A Torres (2026)

Evolutionary Integration and Glucocorticoid Regulation of the Respiratory System: Structure, Function, and Homeostatic Adaptation.

Medical sciences (Basel, Switzerland), 14(1): pii:medsci14010090.

The vertebrate respiratory system arose under evolutionary pressures that linked increasing atmospheric oxygen levels to the metabolic demands of mitochondria. This transition-from ancestral gill-based exchange to the highly alveolated mammalian lung-was accompanied by the emergence of a hormonal regulatory axis centered on the glucocorticoid receptor alpha (GRα). Over time, GRα became deeply integrated into the architecture and function of the respiratory system, aligning pulmonary performance with organismal homeostasis across different developmental stages, environmental challenges, and disease states. This review combines evolutionary, embryological, and molecular evidence to explain how GRα shapes respiratory structure and function. We trace the evolution from ancient oxygen-sensing systems to mammalian alveoli and endothelial adaptations, demonstrating how conserved developmental pathways (including WNT, FGF, BMP, and SHH) are repurposed during both organogenesis and repair. Genetic models show that GRα is essential for preparing the lung for postnatal life, coordinating the reciprocal signaling between mesenchyme and epithelium that drives branching, septation, extracellular matrix organization, and the development of functional alveolar units. In the mature lung, GRα maintains the stability of the alveolar-capillary interface and coordinates immune, vascular, and metabolic functions to support efficient gas exchange. Its actions also extend to red blood cell biology and the regulation of stress erythropoiesis, linking pulmonary oxygen management with systemic oxygen delivery. Mechanistically, GRα interacts with circadian and hypoxia pathways and activates mitochondrial programs that enhance energy production and redox homeostasis during stress. By integrating these regulatory layers across developmental and physiological contexts, this review reframes GRα not simply as a stress-response receptor but as a non-redundant system-level integrator of respiratory homeostasis. Understanding this layered control not only explains the benefits of antenatal corticosteroids but also highlights the therapeutic value of phase-specific, precision modulation of the GC-GRα axis-along with strategies that support GC-GR signaling-to reestablishing and maintaining homeostasis in acute and chronic pulmonary disorders.

RevDate: 2026-02-19
CmpDate: 2026-02-19

Yang C, Luo C, Wang Q, et al (2026)

Insight into the Evolution of Mitochondrial Genetic Basis of Amphibious Adaptation in the Goby (Teleostei: Gobiidae).

Journal of molecular evolution, 94(1):3-13.

The adaptation to terrestrial environments from aquatic environments has always been regarded as a major evolutionary transition in fishes, during which it has been accompanied with diverse phenotypic innovations. Mitochondrial energy metabolism fundamentally enables this shift, but the evolutionary trajectory and molecular mechanisms of mitogenomic adaptations to energy demands are poorly characterized. Mudskippers, a group of gobies with amphibious adaptive traits, serve as ideal models for studying energy metabolism during the water-to-land transition. To test whether amphibious adaptation in gobies corresponds to adaptive evolution in mitochondrial OXPHOS genes, we performed an in silico analysis of the 13 OXPHOS genes from the mitochondrial genomes of 33 goby species and two outgroups. The results showed that: (1) No matter ML or BI methods, four subfamilies Amblyopinae, Gobiinae, Gobionellinae, Oxudercinae are paraphyletic origin, except for subfamily Sicydiinae; besides, genus Scartelaos was first confirmed that it is paraphyletic origin. (2) 13 OXPHOS genes have been under the strong selective constraints, yet, the episodic positive selection was also detected, and ND4 and ATP8 evolution has been found to be under the accelerated evolution. Interestingly, (3) Significant divergent selection was detected between amphibious and fully aquatic lineages in 11 of the 13 OXPHOS genes (84%). And (4) the much stronger selective constraints were uncovered in amphibious lineages. To sum up, OXPHOS genes have undergone adaptive evolution with notable divergent patterns associated with the water-to-land transition during transition from water to land. These results provided some new insights into the genetic basis of amphibious adaptation in goby.

RevDate: 2026-02-19
CmpDate: 2026-02-19

Zhao Z, Ma J, Yang Q, et al (2026)

First Report on Presence of Mitochondrial Introns in Freshwater Sponges, and Pseudogenic Evidence of Their Loss.

Journal of molecular evolution, 94(1):19-23.

Mitochondrial introns have a patchy distribution in sponge lineages. Here, we report on the finding of a group-II-intron in Eunapius rarus (Demospongiae, Spongillidae), which constitutes the first report of a mitochondrial intron in freshwater sponges. Group-II-introns are self-splicing ribozymes, and are particularly rare among sponge mitochondrial genomes. The intron contains complete open reading frames (ORFs), including typical intron-encoded proteins (IEPs). Phylogenetic analysis reveals that the intron is more closely related to those found in brown algae, and distant from other sponge group-II-introns, indicating an acquisition of this intron independent from other sponges. Remarkably, the congeneric E. fragilis does not possess this intron in their mitochondrial genome. However, we found pseudogenic copies of the E. rarus group-II-intron in the nuclear genome of E. fragilis, which indicates patterns of group-II-intron presence and their pseudogene transposition into the nuclear genomes in sponges for the first time. Our results show that a group-II-intron must have been present in the last common ancestor of both Eunapius mt genomes, and subsequently lost in E. fragilis, rather than independent acquisition. Consequently, our findings provide an explanation for the patchy distribution of introns in sponges as a result of frequent losses, besides multiple acquisitions.

RevDate: 2026-02-18

Meneses-Plascencia J, Moreno-Méndez E, Ascencio D, et al (2026)

Metformin-induced longevity is associated with retrotransposon dynamics in yeast chronological aging.

Mechanisms of ageing and development pii:S0047-6374(26)00014-X [Epub ahead of print].

The widely used antidiabetic drug metformin promotes longevity across diverse model organisms, from yeast to primates, yet the cellular mechanisms by which it acts are not fully resolved. Here, we use high-resolution genetic profiling to define metformin's impact on the chronological lifespan of Saccharomyces cerevisiae. Unexpectedly, our analyses uncover pronounced gene-drug interactions between metformin and chromatin modification. In particular, impairment of the histone deacetylase Set3C phenocopies the effects of metformin, suggesting convergence on a shared pathway. Consistent with this genetic interaction, transcriptome sequencing shows that metformin reprograms stationary-phase gene expression, with Ty1-copia retrotransposons emerging as a dominant signature. Notably, targeted analysis of Ty1 expression reveals that Set3C perturbation reproduces the metformin-induced Ty1 response, directly linking chromatin regulation to the observed lifespan phenotypes. Despite this transcriptional activation, metformin reduces TYA Gag-like protein levels without increasing insertion frequency, revealing an uncoupling between retrotransposon expression and mobility. In parallel, proteome analysis identifies increased mitochondrial and stress-response proteins as early outcomes of metformin exposure, both known modulators of Ty1 dynamics and potential mediators of this response. Together, our findings position chromatin regulation and retrotransposon expression as integral components of metformin's effects on longevity, expanding its influence beyond signaling, metabolism, and stress response.

RevDate: 2026-02-18

Zhou J, Wu Q, Wu L, et al (2026)

Nematode-Trapping Devices of Arthrobotrys oligospora is an Iron Storage System Mediated by Elevated Temperatures.

FEMS microbiology ecology pii:8489720 [Epub ahead of print].

Under low-nutrient conditions, nematode-trapping fungi (NTFs) can differentiate their mycelia into specialized trapping devices for capturing prey. Using energy-dispersive X-ray spectroscopy (EDX) in conjunction with transmission electron microscopy (TEM), together with a series of bioassay, we identified that the characteristic electron-dense bodies in trapping devices contained more iron than vacuoles and mitochondria, functioning as an unrecognized iron storage organelle. Genomic analysis revealed that all NTFs lack the Ccc1-mediated vacuolar iron detoxification mechanism conserved in most fungi. Heterogenous expression of yeast-derived Ccc1 gene in A. oligospora significantly reduced trapping device formation and nematicidal activity. Mapping key factor fluctuations onto Bayesian relaxed molecular clock analysis indicated that the loss of Ccc1-mediated vacuolar iron storage occurred during Late Paleozoic Ice Age, whereas the emergence of trapping devices and the acquisition of desferriferrichrome were closely associated with elevated temperatures. Temperature bioassays showed that trap formation is highly temperature-dependent, with free iron levels inversely correlated with temperature, consistent with the temperature sensitivity of A. oligospora, which cannot grow above 30 °C. Our findings demonstrated that global temperature fluctuations serve as a critical driver of the evolution of NTFs and act as a catalyst for the emergence of trapping devices, novel phenotypic indicator of eukaryotic iron overload.

RevDate: 2026-02-17

Grover-Thomas F, van Dorp L, Balloux F, et al (2026)

Climate associated natural selection in the human mito-chondrial genome.

Molecular biology and evolution pii:8488944 [Epub ahead of print].

Mitochondria are essential for cellular energy production and biosynthesis, thermogenesis, and cell signalling, and thus help coordinate physiological responses to changing environments. Humans (Homo sapiens) have adapted to cope with a wide range of climatic conditions, however the role of the mitochondrial genome (mtDNA) in mediating this process remains poorly understood. Here we curated a dataset of 19,570 publicly available full human mitochondrial genomes, an approximate 40-fold increase on earlier studies, paired with modern climate and reconstructed paleoclimate variables. Using a Generalised Linear Model approach, we identify independent candidate variants significantly associated with climatic conditions, suggesting local adaptation in human mitochondrial genomes. Candidate variants are distributed across multiple loci in regulatory, tRNA, rRNA and protein-coding regions - including prominently in ND2 and ND4 complex I subunits. Specific variants are predicted to impact mtDNA transcription, ribosome or protein structure, and multiple have been associated with disease pathologies. We further show that candidate variant genotype distributions are each best modelled by different paleo-bioclimatic variables, consistent with environmental stressors linked to our measured variables exerting subtly distinct selective effects. These stressors may reflect dietary changes or different thermogenic demands at lower temperatures. Our results provide genetic evidence to support the accumulating body of work from functional studies that mitochondria can modulate adaptation to diverse environments. This work underscores the importance of mtDNA in evolutionary biology and its relevance for understanding both disease and physiological variation in global populations.

RevDate: 2026-02-16
CmpDate: 2026-02-16

Chen P, Liu G, Yin J, et al (2026)

Therapeutic Promise of Mitophagy in Cancer: Advancing from Small-Molecule Regulation to Nanotechnology-Enhanced Targeting Therapy.

Theranostics, 16(8):4308-4335.

Mitophagy, a selective autophagic pathway that clears damaged or dysfunctional mitochondria, has emerged as a promising therapeutic approach. Mitophagy maintains a delicate balance between cell survival and death, while mounting evidence suggests that it predominantly promotes tumor cell survival under stress, particularly in responses to cancer therapy. Moreover, aberrant regulation of mitophagy results in cancer pathology with characteristic hallmarks, including remodeling of metabolic plasticity, maintenance of cancer stem cell characteristics, and immune regulation of the tumor microenvironment. This review synthesizes multifaceted roles of mitophagy in cancer biology, from tumor initiation and progression to therapy responses. It also summarizes molecular mechanisms underlying mitophagy. How cancer cells exploit mitophagy to survive therapy has been harnessed to develop therapeutic strategies. We elaborate the evolution of mitophagic therapy from small-molecule modulators to nanotechnology-based targeted delivery systems. Finally, we highlight the promise of targeting mitophagy in overcoming treatment resistance and improving clinical outcomes for patients.

RevDate: 2026-02-16
CmpDate: 2026-02-16

Zhang J, Zhao Z, Xiang T, et al (2026)

From knowledge landscapes to network mechanisms: charting regulated cell death pathways in ALS.

Frontiers in aging neuroscience, 18:1742805.

OBJECTIVE: To map the research landscape linking amyotrophic lateral sclerosis (ALS) with regulated cell death (RCD) and to integrate bibliometric trends with bioinformatics evidence to identify convergent mechanisms and actionable targets.

METHODS: Web of Science Core Collection, PubMed, and Scopus were searched for 2005-2024 (English; Article/Review). After merging and de-duplication, 6,272 records were analyzed using CiteSpace, VOSviewer, and bibliometrix to evaluate publication trends, collaboration, co-citation structure, and keyword evolution. In parallel, ALS-related genes were intersected with apoptosis-, ferroptosis-, and pyroptosis-associated gene sets. Shared targets were used to construct PPI networks, identify core modules and hub genes, and perform GO/KEGG enrichment analyses.

RESULTS: Publications and citations increased steadily with a clear rise after 2015. The field is anchored by the USA and shows rapidly growing contributions from Asia and Europe. Keyword evolution indicates a shift from "oxidative stress/apoptosis" toward multi-pathway RCD, with prominent recent bursts in ferroptosis, pyroptosis, necroptosis, and autophagy/mitophagy, alongside persistent themes in motor-neuron degeneration, mitochondria, and neuro-inflammation. Bio-informatics results showed substantial genetic overlap between ALS and RCD modalities. Hub-gene analysis highlighted TP53, AKT1, STAT3, MYC, RELA, EP300, CREBBP, JUN, HSP90AA1, and MAPK3 as central nodes. Enrichment analyses implicated FoxO, HIF-1, and lipid-related pathways, and GO terms related to chemical/oxidative stress responses and autophagy regulation.

CONCLUSION: ALS-cell death research is consolidating around interconnected RCD programs. Integrated bibliometric and bioinformatics evidence supports an immunometabolic convergence involving ferroptosis-inflammation-autophagy signaling, providing a focused set of candidate pathways and hub targets for mechanistic validation and translation.

RevDate: 2026-02-15

Ruan H, Chen Y, Qian J, et al (2026)

Advances in metal-organic framework-based drug delivery system in cuproptosis-mediated cancer therapy.

European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V pii:S0939-6411(26)00042-1 [Epub ahead of print].

Cancer continues to pose an immense burden on global health, ranking among the foremost causes of disease-associated mortality. Conventional diagnostic platforms for tumor biomarkers, while widely adopted, remain constrained by limited sensitivity, protracted workflows, and substantial economic costs, thereby restricting their clinical applicability. Therapeutic modalities such as chemotherapy and radiotherapy further compound the challenge, offering only modest selectivity and being accompanied by significant systemic toxicity and a high likelihood of relapse. Metal-organic frameworks (MOFs) represent a class of structurally tailorable nanomaterials composed of modular building units, featuring tunable porosity and favourable biocompatibility, which together provide an efficient platform for drug encapsulation and controlled release. Their tumour accumulation behaviour is strongly governed by key physicochemical parameters, including particle size, morphology, and surface chemistry. Pristine MOFs primarily rely on passive tumour targeting through the enhanced permeability and retention effect, whereas surface functionalization with targeting ligands can markedly improve tumor selective enrichment and cellular uptake. Consequently, the therapeutic delivery performance of MOFs must be critically assessed in relation to their specific structural design and surface engineering strategies. In parallel, the identification of cuproptosis, a mitochondria-centered copper-dependent mode of regulated cell death, has opened a distinct mechanistic avenue for oncological intervention. This process arises from the aberrant interaction of copper ions with lipoylated tricarboxylic acid cycle proteins, culminating in excessive protein acylation, destabilization of Fe-S cluster enzymes, proteotoxic stress, and mitochondrial collapse. The rapid evolution of pharmacological agents exploiting this pathway underscores its transformative therapeutic potential. This review critically consolidates recent progress at the interface of MOFs and cuproptosis, emphasizing design strategies, mechanistic insights, and therapeutic deployment, while also addressing unresolved issues in pharmacokinetics, biosafety, and translational feasibility that must be overcome for clinical realization.

RevDate: 2026-02-13
CmpDate: 2026-02-13

Shemarova IV, ER Nikitina (2026)

Mechanisms of Protection Against Oxidative Stress During Hibernation.

International journal of molecular sciences, 27(3): pii:ijms27031319.

Hibernation-the ability of some animals to enter prolonged winter sleep-is a natural hypometabolic state that allows them to withstand adverse environmental factors (low temperatures, food and water shortages). The ability to hibernate is a consequence of adaptations accumulated over evolution at various physiological levels, among which molecular adaptation to hypoxia plays a key role, which eliminates not only the negative effect of oxygen deficiency on cells, but also the danger of oxidative stress (OS) after awakening. This aspect of hibernation is medically important because understanding the mechanisms underlying the adaptation of hibernating animals to hypoxia and OS can help address a number of important issues related to preventing post-hypoxic complications in people with chronic neurodegenerative and heart disease. The molecular basis of adaptation to hypoxia in hibernating animals is the presence of an effective antioxidant system (AOC) and regulatory mechanisms that provide extraordinary mitochondrial plasticity, which is especially pronounced when animals emerge from hibernation. This review summarizes and systematizes the latest advances in the study of mitochondria and antioxidant defenses during mammalian hibernation, primarily gophers-a common experimental model of hibernation.

RevDate: 2026-02-12

Shahbazi M, Sharbrough J, Knerova J, et al (2026)

Causes and Consequences of Cytonuclear Incompatibility in Hybrids of Flowering Plants.

Journal of experimental botany pii:8475166 [Epub ahead of print].

Hybridization and polyploidization combine divergent nuclear genomes with maternally inherited organelles, often disrupting cytonuclear coadaptation critical for respiration and photosynthesis. This review examines the mechanisms, outcomes, and evolutionary significance of cytonuclear incompatibility in plants. We focus on how divergence in nuclear-encoded, organelle-targeted proteins and organelle genomes leads to mismatched interactions in protein import, folding, and assembly of multi-subunit enzyme complexes. The evidence highlights taxon- and complex-specific responses that mitigate incompatibilities, including the biased retention and expression of maternal alleles, gene conversions, and regulatory adjustments. We highlight how cytonuclear compatibility in hybrid lineages entails responses at multiple levels of regulation, including methylation/chromatin accessibility, gene expression, alternative splicing, translation rates, organelle import, protein-folding and assembly, and protein degradation pathways. Manifestations such as chlorosis, seed sterility, or hybrid breakdown underscore their role in shaping reproductive barriers. Conversely, maternal bias and compensatory mechanisms often act to restore functional integration of parental genomes, allowing hybrid and polyploid persistence. Beyond their evolutionary role in speciation and adaptation, cytonuclear incompatibilities underpin key practical applications, notably cytoplasmic male sterility, a cornerstone of hybrid crop breeding. We conclude that cytonuclear dynamics reveal both constraints and opportunities, illuminating plant diversification, hybrid resilience, and agricultural innovation.

RevDate: 2026-02-10

Intarasit S, S Inwongwan (2026)

Coordinating photosynthesis and respiration: Evolution and functional integration of mitochondria and chloroplasts in algae.

Plant physiology pii:8470586 [Epub ahead of print].

The coordination of photosynthesis and respiration is central to cellular energy balance, yet in algae this relationship exhibits exceptional diversity. Shaped by successive endosymbioses, algal lineages represent natural experiments in merging two energy systems of distinct bacterial ancestry: the chloroplast and the mitochondrion. Their structural proximity, shared redox pathways, and dual-targeted proteins enable dynamic communication between photosynthetic and respiratory metabolism. Recent imaging and multi-omics studies reveal that this interaction is highly responsive to environmental variables such as light intensity, nutrient availability, and oxidative stress. In diatoms, mitochondria envelop the plastid to exchange ATP and reducing power, whereas in green algae and euglenoids, malate/oxaloacetate shuttles, alternative oxidases, and cyclic electron flow collectively stabilize chloroplast redox states. This functional coupling optimizes CO2 fixation and photoprotection under stress and underlies the metabolic flexibility of mixotrophic species such as Euglena gracilis. This review synthesizes the current understanding of mitochondria-chloroplast integration in algae from evolutionary, structural, and mechanistic perspectives, highlighting photosynthesis-respiration coordination as a unifying physiological principle. By elucidating how inter-organelle networks sustain carbon assimilation and redox homeostasis, these insights advance our understanding of algal productivity and resilience and inform strategies for improving energy efficiency in photosynthetic systems.

RevDate: 2026-02-10
CmpDate: 2026-02-10

Lee S, Chakraborty S, Kim S, et al (2026)

Organelles harbour pH gradients.

Research square.

Organelle pH is critical to organelle identity and function. Resident proteins that define each organelle modify transiting cargo proteins, with both retention and trafficking between organelles governed by pH-dependent mechanisms. For example, lysosomal enzymes bind mannose-6-phosphate receptors at the higher pH (~6.5) of the Golgi and dissociate at the lower pH (~5.5) of late endosomes[1]. Proteins that stray from the endoplasmic reticulum (ER) are captured by KDEL receptors in the acidic Golgi and returned into the neutral ER[2,3]. This pH-tuned trafficking system compartmentalizes organelle function and prevents mis-localization of critical enzymes[4]. Dysregulated organelle pH disrupts their function and leads to various diseases. Because protons move rapidly in water, the pH within a single organelle is currently assumed to be spatially uniform[5]. Here, using a reporter sensitive from pH 5.5 - 10.5 to map a spectrum of organelles at high resolution, we discovered that pH gradients exist within single, large or long organelles such as the ER and mitochondria, and in membrane-less organelles without ion-transporting proteins such as the nucleolus. These new findings upend our understanding of organellar pH, prompting new questions about proton diffusion within the cell, and its potential consequences on organelle function.

RevDate: 2026-02-05
CmpDate: 2026-02-05

Tobiasson V, Luo J, Wolf YI, et al (2026)

Dominant contribution of Asgard archaea to eukaryogenesis.

Nature, 650(8100):141-149.

The origin of eukaryotes is one of the key problems in evolutionary biology[1,2]. The demonstration that the last eukaryotic common ancestor (LECA) already contained the mitochondrion-an endosymbiotic organelle derived from an alphaproteobacterium-and the discovery of Asgard archaea-the closest archaeal relatives of eukaryotes[3-7]-inform and constrain evolutionary scenarios of eukaryogenesis[8]. We conducted a comprehensive analysis of the origins of core eukaryotic genes tracing to the LECA within a rigorous statistical framework centred around evolutionary hypothesis testing using constrained phylogenetic trees. The results show dominant contributions of Asgard archaea to the origin of most of the conserved eukaryotic functional systems and pathways. A limited contribution from Alphaproteobacteria was identified, relating primarily to energy transformation systems and Fe-S cluster biogenesis, whereas ancestry from other bacterial phyla was scattered across the eukaryotic functional landscape, without clear, consistent trends. These findings imply a model of eukaryogenesis in which key features of eukaryotic cell organization evolved in the Asgard lineage leading to the LECA, followed by the capture of the alphaproteobacterial endosymbiont and augmented by numerous but sporadic horizontal acquisitions of genes from other bacteria both before and after endosymbiosis.

RevDate: 2026-02-04

Varikasuvu SR (2026)

Mitochondria and Moon: Footprints Shaping Life's Evolution and Cosmic Exploration.

Advances in physiology education [Epub ahead of print].

This Viewpoint explores a novel and striking analogy between mitochondrial cristae and lunar footprints, highlighting both visual and conceptual parallels. By integrating metaphor, and connecting cellular architecture with human exploration, it illustrates how enduring imprints mark milestones in evolution and discovery. The analogy offers a perspective for teaching physiology that links structure and function with imagination and interdisciplinary thinking. Students can better appreciate how microscopic cellular features reflect evolutionary milestones while recognizing that scientific inquiry, whether at the cellular or cosmic scale, is driven by the same human desire to know and to advance.

RevDate: 2026-02-04
CmpDate: 2026-02-04

Zhu Q, Zhang J, Zhou W, et al (2026)

Introgressed mitochondrial fragments from archaic hominins alter nuclear genome function in modern humans.

Science advances, 12(6):eaea0706.

Archaic introgression introduced functionally relevant variants into modern humans, yet small-scale insertions remain understudied. Here, we leverage 2519 modern human genomes and four high-coverage archaic hominin genomes to systematically characterize nuclear mitochondrial DNA segments (NUMTs). We uncover 483 polymorphic NUMTs across globally diverse human populations and 10 in archaic genomes. By combining overlap with Neanderthal-derived and Denisovan-derived haplotypes, phylogenetic analyses, insertion time estimates, and haplotype colocalization, we identify five NUMTs introduced into modern humans via archaic hominin introgression. Functional analyses reveal that introgressed NUMTs can modulate gene expression, including allele-specific up-regulation of the immune-related gene RASGRP3, and reshape three-dimensional chromatin structure at loci such as SCD5 and HNRNPD. These findings highlight an underappreciated mechanism by which archaic mitochondrial fragments shape nuclear genome function and evolution. Our study reframes NUMTs not as passive genomic fossils but as dynamic elements influencing modern human diversity and adaptation.

RevDate: 2026-02-04
CmpDate: 2026-02-04

Kay CJ, Spang A, Szöllősi GJ, et al (2026)

Dated gene duplications elucidate the evolutionary assembly of eukaryotes.

Nature, 650(8100):129-140.

The origin of eukaryotes was a formative but poorly understood event in the history of life. Current hypotheses of eukaryogenesis differ principally in the timing of mitochondrial endosymbiosis relative to the acquisition of other eukaryote novelties[1]. Discriminating among these hypotheses has been challenging, because there are no living lineages representative of intermediate steps within eukaryogenesis. However, many eukaryotic cell functions are contingent on genes that emerged from duplication events during eukaryogenesis[2,3]. Consequently, the timescale of these duplications can provide insights into the sequence of steps in the evolutionary assembly of the eukaryotic cell. Here we show, using a relaxed molecular clock[4], that the process of eukaryogenesis spanned the Mesoarchaean to late Palaeoproterozoic eras. Within these constraints, we dated the timing of these gene duplications, revealing that the eukaryotic host cell already had complex cellular features before mitochondrial endosymbiosis, including an elaborated cytoskeleton, membrane trafficking, endomembrane, phagocytotic machinery and a nucleus, all between 3.0 and 2.25 billion years ago, after which mitochondrial endosymbiosis occurred. Our results enable us to reject mitochondrion-early scenarios of eukaryogenesis[5], instead supporting a complexified-archaean, late-mitochondrion sequence for the assembly of eukaryote characteristics. Our inference of a complex archaeal host cell is compatible with hypotheses on the adaptive benefits of syntrophy[6,7] in oceans that would have remained largely anoxic for more than a billion years[8,9].

RevDate: 2026-02-03

Tan HX, Gao QH, X Tong (2026)

The morphology of male accessory glands in the Glenea cantor (Fabricius, 1787) (Coleoptera: Cerambycidae: Lamiinae).

Micron (Oxford, England : 1993), 203:103999 pii:S0968-4328(26)00013-2 [Epub ahead of print].

Male accessory glands of insects serve as secretory organs, exhibiting the ability to produce secretions that regulate reproductive processes. Their histology and ultrastructure are generally regarded as being diverse within insect groups, however, as one of the largest groups of insects, the ultrastructure of male accessory glands in Cerambycidae has never received sufficient attention. The longhorn beetle Glenea cantor (Fabricius, 1787) (Coleoptera: Cerambycidae: Lamiinae) is a wood-boring pest infesting urban landscape trees in southern China, significantly compromising urban greening. In this study, light and transmission electron microscopes were used to reveal the histological and ultrastructural characteristics of the male accessory glands of G. cantor. Results show that the males of G. cantor possess two pairs of morphologically distinct mesodermal glands (mesadenia). One pair exhibits an overall elongated tubular shape, while the other displays a tightly coiled, clew-like structure proximally and free-ending tubular regions distally. Ultrastructurally, both pairs of mesadenia exhibit identical cell types, with abundant secretory granules observed within the cytoplasm and lumen. Each gland possesses a muscular layer, an epithelium, and a lumen. The epithelial cell layer contains cellular structures and organelles indicative of active protein synthesis, including rough endoplasmic reticulum (RER), mitochondria, Golgi appartus, and secretory vesicles. This epithelium is also characterized by the presence of microvilli. The lumen is filled with electron-dense secretion. Notably, distinct morphological and ultrastructural differences exist both between the two mesadenial pairs and within each pair between their proximal and distal regions. This study provides the first comparative morphological and ultrastructural analysis of regional differentiation in two pairs of male accessory glands of G. cantor, revealing adaptive changes acquired during their evolution.

RevDate: 2026-02-03
CmpDate: 2026-02-03

Lim SJ, M Breitbart (2026)

Genetic Features of the Scuticociliate Pathogen Philaster sp. Isolate FWC2 That Causes Sea Urchin Mass Mortality.

The Journal of eukaryotic microbiology, 73(2):e70065.

A scuticociliate most closely related to Philaster apodigitiformis caused mass mortalities of diadematoid sea urchins and was cultured as Philaster sp. isolate FWC2. We sequenced the metagenomic content of this isolate, which was predicted to represent ≤ 56% of the complete genome. Based on k-mer counts, the haploid genome size was predicted to be 122-136 Mbp. We assembled and annotated a 4,088 bp nuclear ribosomal operon, a 41,396 bp mitochondrial genome with 19.22% G + C content, 24 protein-coding genes, 6 tRNA genes, and 2 rRNA genes, and a protein sequence homologous to β-PKA in Philaster apodigitiformis potentially involved in host infection.

RevDate: 2026-02-03
CmpDate: 2026-02-03

Li G, Zhang Y, Yu H, et al (2026)

A tripartite pollen killer-protector system confers temperature-sensitive inter-subspecific reproductive isolation in rice.

Molecular plant, 19(2):295-312.

Hybrid-sterility-mediated reproductive isolation is pivotal for speciation, yet the underlying molecular mechanisms and environmental responses remain unclear. Here, we report a temperature-sensitive pollen killer-protector system at a three-gene Sa locus for indica-japonica rice hybrid sterility. Genetic analyses identified SaFL[+], a strong pollen protector from Sa-i (indica allele), and SaFL[-], a weak japonica allele from Sa-j, which is exclusively functional under high temperatures. Protein interaction, ubiquitination, and degradation assays showed that SaF[+] and SaM[+] from Sa-i form a pollen-killer complex to bind and ubiquitinate the reactive oxygen species scavenger COX11 for degradation in mitochondria, causing male sterility of the Sa-j pollen. Protein affinity and competitive binding assays indicated that in the Sa-i pollen, SaFL[+] binds SaM[+] to disrupt the killer complex and restore fertility. However, the weak protector SaFL[-] can bind SaM[+] under high temperatures, sparing the Sa-j pollen from sterility. Synteny comparisons and haplotype analyses showed that the Sa locus originated in ancient wild rice and underwent divergence within the Oryza genus during expansion from tropical to temperate environments, which might have driven latitudinal adaptation and reproductive isolation in rice populations. Thus, Sa represents a temperature-sensitive reproductive-isolation system associated with domestication and environmental adaptation in rice.

RevDate: 2026-02-02
CmpDate: 2026-02-02

Saldamando CI, Candamil-Cortés MS, Rodríguez-Cabal HA, et al (2026)

Genomic and phylogenetic insights for three species of thrips (Thysanoptera: Terebrantia) associated with Colombian avocado.

Journal of insect science (Online), 26(1):.

Thrips are small, cosmopolitan pests that attack a wide variety of crops, including avocado (Persea americana Mill.), where they feed on the fruit surface, hindering export quality. In Colombia, 7 thrips species have been identified in avocado where Frankliniella gardeniae (Fg) (Moulton, 1948), F. panamensis (Fp) (Hood, 1925), and Scirtothrips hansoni (Sh) (Mound and Hoddle, 2016) are the most abundant. Despite their economic importance, limited genomic and transcriptomic data are available for these pests. Here, we present the first draft genomes of these species and compare them to the reference genome of Frankliniella occidentalis. The mitochondrial genomes (mitogenomes) of the 3 species differ in size and gene order, with F. gardeniae exhibiting the largest mitochondria. Phylogenetic analysis clustered F. gardeniae and F. panamensis together and S. hansoni with S. dorsalis. Genome assembly revealed differences in genome sizes: 397 Mbp (Fp), 454 Mbp (Sh), and 601 Mbp (Fg), with F. gardeniae having the largest genome. Coverage was 118× for S. hansoni and 35× for the other 2 species. S. hansoni showed the highest sequence count and N50 values. BUSCO analysis estimated genome completeness between 96% and 97.95%. Annotated genes shared among these species included insecticide resistance and metabolism, particularly P450 and CYP family genes, as well as chemosensory genes (Ir). They are promising targets for RNA interference-based studies to enhance pest management strategies thus further studies are required in this issue.

RevDate: 2026-02-02
CmpDate: 2026-02-02

Łabędzka-Dmoch K, Bui THD, Piątkowski J, et al (2026)

Mitochondrial retrograde control of transcription evolves with respiratory stress, metabolic adaptation, and virulence in budding yeasts.

Molecular biology and evolution, 43(2):.

The pathway involving the paralogous transcription factors Rtg1 and Rtg3 was first described in Saccharomyces cerevisiae as the retrograde regulation that adapts cellular metabolism in response to the state of mitochondrial respiration. We investigated the evolution of this pathway by studying its target genes in respiratory-deficient mutants of Candida albicans-a phylogenetically distant and metabolically distinct yeast species. We show that in C. albicans the Rtg pathway is also responsible for adaptation to cellular stresses related to respiratory dysfunction, but the repertoire of its target genes is different than in S. cerevisiae, and includes genes encoding proteins involved in alternative respiration, oxidative stress, mitophagy, and other aspects of metabolism. We also traced the evolution of the main components of the Rtg pathway and its target genes in the budding yeast (Saccharomycotina) subphylum. We show that the system originated within this clade following a single duplication of the gene encoding the ancestor of Rtg1 and Rtg3, but employs other factors, like the regulatory proteins Rtg2 and Mks1 that were likely present in the last common ancestor of budding yeasts. The regulation of the Rtg transcription factors in C. albicans is different than in S. cerevisiae, as both Rtg2 and Mks1 were lost in the majority of Serinales. Among the target genes, of particular interest is the evolution of the alternative oxidase (Aox), which was either lost or duplicated in multiple independent events. The presence of Aox strongly correlates with the mitochondrially encoded Complex I-a major source of oxidative stress.

RevDate: 2026-01-31
CmpDate: 2026-01-31

Shao BY, Liu SJ, Zhang TQ, et al (2026)

Mitochondrial genomes of Mentha reveal structural complexity and evolutionary diversity.

Molecular genetics and genomics : MGG, 301(1):25.

Mitochondrial genomes play essential roles in plant energy metabolism and evolution, yet their structural complexity and diversity in plants remain poorly understood. This study aims to address the question by analyzing four newly assembled Mentha mitochondrial genomes (M. longifolia, M. suaveolens, M. pulegium, and M. requienii), which serve as valuable genomic resources for phylogenetic and evolutionary studies. Comparative analyses revealed structural diversity, codon usage bias, extensive RNA editing, and abundant repetitive sequences driving genomic rearrangements in the four mitochondrial genomes. Chloroplast-derived DNA fragments were dynamically integrated into the four Mentha mitochondrial genomes, highlighting ongoing interorganellar DNA transfer between plastids and mitochondria. Phylogenetic reconstructions based on mitochondrial, nuclear, and chloroplast genomes exhibit considerable discordance, reflecting complex evolutionary processes such as hybridization, introgression, and allopolyploidization within the genus. In conclusion, the structural diversity, codon usage bias, and ongoing interorganellar DNA transfer observed in Mentha mitochondrial genomes underscore their dynamic evolutionary nature. The discordance among mitochondrial, plastid, and nuclear phylogenies reflects complex evolutionary processes (possibly hybridization and allo-polyplodization) of Mentha species. These findings enhance the understanding of the mechanisms underlying the complexity and diversity of Mentha species and provide broader insights into the evolution of plant mitochondrial genomes.

RevDate: 2026-01-31

Shelake RM, Waghunde RR, JY Kim (2026)

Coevolution of plant-microbe interactions, friend-foe continuum, and microbiome engineering for a sustainable future.

Molecular plant pii:S1674-2052(26)00011-0 [Epub ahead of print].

The coevolution of plant-microbe (PM) associations over approximately 450 million years has been a fundamental driver of terrestrial life, giving rise to mutualistic, commensal, and pathogenic relationships along a dynamic friend-foe continuum. The need to adapt to the host environment has driven the convergent evolution of common strategies among mutualists and pathogens, enabling them to evade or modulate the plant immune system. This review synthesizes PM coevolution within a deep-time, three-pillar framework: organellogenesis, root evolution, and immune gatekeeping, linking ancient endosymbiotic events (mitochondria, chloroplast, and nitroplast) to contemporary holobiont-level phenotypes and biotechnological applications. We organize the friend-foe continuum around a coevolution-guided cost-benefit and tipping-point framework, using identified molecular switches and evolutionary constraints to derive actionable design rules for engineering PM associations. Moving beyond a descriptive toolbox of technologies, we integrate recent breakthroughs to analyze how four principal axes: host and microbial genetics, evolutionary dynamics, environmental and ecological conditions, and metabolic switches define the thresholds that govern microbial lifestyle transitions. Finally, we propose specific, testable strategies for PM coevolution-informed crop improvement, distinguishing near-term feasible targets from long-term speculative goals in nitrogen utilization, synthetic microbial communities, immune receptor engineering, modulation of plant memory, and microbiome-integrated breeding through genome editing, synthetic biology, AI, and microbiome engineering. Together, these approaches extend existing syntheses into a predictive, evolution-informed framework that transforms coevolutionary principles into a functional blueprint for sustainable and resilient agriculture.

RevDate: 2026-01-30

Bertschmann J, Liu G, Djamshidi M, et al (2026)

A recently evolved domain of the human ING1 epigenetic regulator targets mitochondria and induces senescence.

Cellular and molecular life sciences : CMLS pii:10.1007/s00018-025-06076-y [Epub ahead of print].

RevDate: 2026-01-30

Acharya S, Hanssen E, Bouwer JC, et al (2026)

Exploring placental ultrastructure: A review of electron microscopy techniques and emerging methods for resolving 3D organelle architecture.

Placenta pii:S0143-4004(26)00021-4 [Epub ahead of print].

Trophoblast cells line the surface of placental villi, facilitating the exchange of nutrients, gases, and wastes between the maternal and fetal circulations. The fusion of cytotrophoblast (CTB) cells into the surrounding multinucleated syncytiotrophoblast (STB), is accompanied by a shift in cellular ultrastructure (subcellular architecture). Mitochondria undergo a remarkable decrease in size and alteration in morphology following trophoblast differentiation, and have thus been the subject of investigations due to their crucial role in producing energy for placental development. Observing this shift in structure has relied on the use of electron microscopy, which has offered insights into underlying mitochondrial functions. Since the initial use of electron microscopy to study villous trophoblasts in the 1950s, novel techniques have emerged that have the capacity to interrogate placental ultrastructure with unprecedented resolution. This review discusses the evolution of electron microscopy techniques to study the placenta over the last 70 years. Moreover, we discuss emerging methods for resolving 3D organelle structure within the placenta, which offer more physiologically pertinent information and context for complex topologies. Further, we discuss advanced methods of cryo-electron tomography (cryo-ET) that present the placental field with an exciting opportunity to determine the complex relationship between mitochondrial architecture and protein structure in the human placenta. By specifically focusing on mitochondrial imaging, we showcase the capacity for volume electron microscopy and cryo-ET to reveal the role of organelle structure in placental development.

RevDate: 2026-01-29

Corre P, Pilátová J, Bílý T, et al (2026)

Energy metabolism and adaptation to hypoxia in the non-photosynthetic green alga Leontynka.

BMC biology pii:10.1186/s12915-026-02529-3 [Epub ahead of print].

BACKGROUND: Leontynka is a non-photosynthetic lineage of the order Chlamydomonadales (Chlorophyta). Although many Chlamydomonadales members encode components of the anaerobic energy metabolism, studies focused on Chlamydomonadales algae thriving in hypoxia and not prospering in oxic conditions are missing. Using a combination of experimental approaches, comparative genomics, and advanced in silico protein localization analyses, we employed Leontynka as a model to investigate the evolution of anaerobiosis in Chlamydomonadales.

RESULTS: Leontynka spp. accumulate a wide range of storage forms, enabling them to cope with nutritional stresses. Their mitochondria contain well-developed cristae mediating a conventional aerobic energy metabolism. Moreover, colocalization of a Raman signal for cytochromes with the position of mitochondria in the cell indicates that oxidative phosphorylation is an important route of energy metabolism in the alga. Interestingly, Leontynka spp. concentrate enzymes potentially involved in oxygen-independent ATP synthesis within the plastid, which lost the ability to produce ATP using proton gradient generated by membrane complexes that exploit redox reactions. We analyzed the composition of prokaryotic communities co-isolated with Leontynka spp. and hypothesize that their preference for hypoxic/microoxic conditions is facilitated by metabolic interactions with certain microaerophilic and anaerobic bacteria.

CONCLUSIONS: This study represents the first comprehensive analysis of microaerophilic Chlamydomonadales algae. Having retained several ancestral enzymes of the anaerobic energy metabolism, Leontynka represents a unique vantage point for understanding the evolution of the hydrogen production machinery and adaptations to low oxygen in Chlamydomonadales (and core chlorophytes in general). Our findings suggest that the plastid of non-photosynthetic Leontynka follows a similar evolutionary path as mitochondria when adapting to anaerobiosis and parallels the transition of a mitochondrion into a hydrogenosome.

RevDate: 2026-01-29
CmpDate: 2026-01-29

Berdun F, Senkler J, Senkler M, et al (2026)

From isolation to insights: mitochondrial complex I in the diatom Phaeodactylum tricornutum.

The Plant journal : for cell and molecular biology, 125(3):e70706.

Diatoms are among the most ecologically successful microalgae, contributing significantly to marine primary production and global carbon cycling. Their distinctive metabolic architecture, shaped by a complex evolutionary history involving secondary endosymbiosis, includes a highly compartmentalized cell organization and unique metabolic pathways. In Phaeodactylum tricornutum, a model pennate diatom, chloroplasts with four membranes and mitochondria of likely exosymbiotic origin exhibit intricate physical and metabolic interactions that support integrated carbon and nitrogen metabolism. The mitochondrial electron transport chain, essential for ATP synthesis, shows clade-specific structural and compositional adaptations. Despite its importance, detailed proteomic characterization has remained limited. Here, we report a method for the isolation of mitochondrial complex I from P. tricornutum and present a comprehensive proteomic analysis. Our results confirm the presence of carbonic anhydrase and bridge modules, both previously proposed as ancestral features of mitochondrial complex I, and identify at least one novel, clade-specific subunit that resembles NAD(P)H-dependent trans-2-enoyl-CoA/ACP reductases (TER) from other species. The subunit is similar to proteins involved in mitochondrial fatty acid biosynthesis. Our findings provide new insights into the composition, evolutionary conservation, and potential biotechnological relevance of this essential respiratory protein complex in diatoms.

RevDate: 2026-01-29

Chen G, Dong H, Y Tian (2026)

Mito-nuclear communication: From cellular responses to organismal health.

Molecular cell pii:S1097-2765(26)00021-3 [Epub ahead of print].

The co-evolution of mitochondria and the nucleus established constant mito-nuclear communication that is essential for both cellular and organismal homeostasis. At the cell-autonomous level, mitochondrial perturbations activate retrograde pathways such as the mitochondrial unfolded protein response (UPR[mt]) and the mitochondrial integrated stress response (ISR[mt]), which couple organelle dysfunction to nuclear transcriptional programs, thereby promoting mitochondrial function and preserving cellular integrity. Importantly, this communication is not confined to individual cells but extends across tissues to coordinate systemic adaptations. Stress signals can be sensed, broadcasted through secreted mitokines and neural circuits, and then interpreted by distal organs to coordinate systemic adaptations. These systemic responses integrate metabolism, immunity, and behavior, conferring resilience to stress and shaping the trajectory of aging. Understanding this multi-layered communication, from the organelle to the organism and its microbial ecosystem, promises new therapeutic strategies to enhance mitochondrial function, promote resilience, and extend healthspan.

RevDate: 2026-01-28
CmpDate: 2026-01-28

Chevret CJL, Echegaray JF, Walton A, et al (2026)

Tissue-specific mitochondrial pathway remodeling linked to longevity in honeybee queens.

PloS one, 21(1):e0341233 pii:PONE-D-25-49904.

Mitochondrial metabolism plays a critical role in determining lifespan across animal taxa. In our study, we used the Western honeybee (Apis mellifera) as a model, capitalizing on the stark lifespan difference between queens, which often live more than two years, and summer workers, which survive only about 30 days, despite sharing the same genetic background. We investigated mitochondrial function in head tissue, thoracic muscle, and abdominal fat tissue of queens and workers, comparing early (7 days) and late adult stages (28-30 days in workers; 2 years in queens). No significant differences in mitochondrial flux control ratio for the NADH- Succinate- and glycerophosphate (Gp) pathways were found in thoracic muscles across castes or age groups. In head and abdominal fat tissues, early-life queens showed reduced reliance on NADH-linked pathways for maximal respiratory flux compared to workers. The decrease in the NADH-pathway was compensated by an increase in the Gp-pathway contribution. Queens exhibited reduced phosphorylation-pathway control over OXPHOS compared to workers, both in head tissue during early life and in abdominal fat tissue later in life. These findings reveal caste- and tissue-specific patterns of mitochondrial regulation that may contribute to dramatic lifespan divergence observed in eusocial insects. They suggest that early-life metabolic flexibility could play an important role in shaping life history evolution in Apis mellifera.

RevDate: 2026-01-28

Cai L, Havird JC, RK Jansen (2026)

Recombination and retroprocessing in broomrapes reveal RNA-mediated gene transfer mechanism and a generalizable model for mitochondrial evolution in heterotrophic plants.

Genome biology and evolution pii:8442980 [Epub ahead of print].

The altered life history strategies of heterotrophic organisms often leave a profound genetic footprint on energy metabolism related functions. In parasitic plants, the reliance on host-derived nutrients and loss of photosynthesis in holoparasites have led to highly degraded to absent plastid genomes, but its impact on mitochondrial genome (mitogenome) evolution has remained controversial. By examining mitogenomes from 45 Orobanchaceae species including three independent transitions to holoparasitism and key evolutionary intermediates, we identified measurable and predictable genetic alterations in genomic shuffling, RNA editing, and intracellular (IGT) and horizontal gene transfer (HGT) en route to a nonphotosynthetic lifestyle. In-depth comparative analyses revealed DNA recombination and repair processes, especially conversion of RNA-mediated retroprocessing, as significant drivers for genome structure evolution. In particular, we identified a novel RNA-mediated IGT and HGT mechanism, which has not been demonstrated previously in cross-species and inter-organelle transfers. We propose a dosage effect mechanism to explain the biased transferability of plastid DNA to mitochondria across green plants, especially in heterotrophic lineages like parasites and mycoheterotrophs. Evolutionary rates scaled with these genomic changes, but the direction and strength of selection varied substantially among genes and clades, resulting in high contingency in mitochondrial genome evolution. Finally, we summarize mitochondrial evolutionary trends in Orobanchaceae that are potentially generalizable to other heterotrophic plants: increased recombination and repair activities, rather than relaxed selection alone, lead to differentiated genome structure compared to free-living species.

RevDate: 2026-01-28
CmpDate: 2026-01-28

Bartusik-Aebisher D, Rogóż K, Henrykowska G, et al (2025)

Advances in Near-Infrared BODIPY Photosensitizers: Design Strategies and Applications in Photodynamic and Photothermal Therapy.

Pharmaceuticals (Basel, Switzerland), 19(1): pii:ph19010053.

Background/Objectives: Boron-dipyrromethene (BODIPY) derivatives are a superior class of fluorophores prized for their exceptional photostability and tunable photophysical properties. While ideal for imaging, their translation to photodynamic therapy (PDT) has been hampered by excitation in the visible range, leading to poor tissue penetration. To overcome this, intense research has focused on developing near-infrared (NIR)-absorbing BODIPY photosensitizers (PS). This review aims to systematically summarize the hierarchical design strategies, from molecular engineering to advanced nanoplatform construction, that underpin the recent progress of NIR-BODIPY PS in therapeutic applications. Methods: We conducted a comprehensive literature review using PubMed, Scopus, and Web of Science databases. The search focused on keywords such as "BODIPY", "aza-BODIPY", "near-infrared", "photodynamic therapy", "photothermal therapy", "nanocarriers", "hypoxia", "immuno-phototherapy", and "antibacterial." This review analyzes key studies describing molecular design, chemical modification strategies (e.g., heavy-atom effect, π-extension), nanoplatform formulation, and therapeutic applications in vitro and in vivo. Results: Our analysis reveals a clear progression in design complexity. At the molecular level, we summarize strategies to enhance selectivity, including active targeting, designing "smart" PS responsive to the tumor microenvironment (TME) (e.g., hypoxia or low pH), and precise subcellular localization (e.g., mitochondria, lysosomes). We then detail the core chemical strategies for achieving NIR absorption and high singlet oxygen yield, including π-extension, the internal heavy-atom effect, and heavy-atom-free mechanisms (e.g., dimerization). The main body of the review categorizes the evolution of advanced theranostic nanoplatforms, including targeted systems, stimuli-responsive 'smart' systems, photo-immunotherapy (PIT) platforms inducing immunogenic cell death (ICD), hypoxia-overcoming systems, and synergistic chemo-phototherapy carriers. Finally, we highlight emerging applications beyond oncology, focusing on the use of NIR-BODIPY PS for antibacterial therapy and biofilm eradication. Conclusions: NIR-BODIPY photosensitizers are a highly versatile and powerful class of theranostic agents. The field is rapidly moving from simple molecules to sophisticated, multifunctional nanoplatforms designed to overcome key clinical hurdles like hypoxia, poor selectivity, and drug resistance. While challenges in scalability and clinical translation remain, the rational design strategies and expanding applications, including in infectious diseases, confirm that NIR-BODIPY derivatives will be foundational to the next generation of precision photomedicine.

RevDate: 2026-01-27

Pandey SK, Kulshreshtha A, A Mishra (2026)

The Role of Mitochondrial Ion Channels in the Evolution of Anticancer Drug Resistance.

Current protein & peptide science pii:CPPS-EPUB-152865 [Epub ahead of print].

Apoptosis, drug resistance, and cellular metabolism are all crucially regulated by mitochondria, especially through ion channels and translocases embedded in their membranes. The outer mitochondrial membrane (OMM) contains the voltage dependent anion channel (VDAC), which acts with proteins such as hexokinase II and BAX to regulate apoptosis and metabolic reprogramming in cancer while facilitating the flow of important metabolites and ions. Anti apoptotic proteins like Bcl2 and Mcl1 closely regulate the mitochondrial apoptosis induced channel (MAC), which is created by pro-apoptotic Bcl2 family members BAX and BAK and controls cytochrome c release when overexpressed, leading to drug resistance. Furthermore, the translocase of the outer membrane (TOM) complex, which regulates mitochondrial protein import, is frequently dysregulated in cancers. Numerous ion channels, such as potassium channels, the mitochondrial calcium uniporter (MCU), and the mitochondrial permeability transition pore (m-PTP), are found within the inner mitochondrial membrane (IMM) and regulate important functions like ATP synthesis, the control of reactive oxygen species (ROS), and apoptotic signaling. Cancer cells can avoid apoptosis, adapt to environmental stress, and become resistant to treatments like doxorubicin and cisplatin when these channels are dysregulated. Metabolic flexibility and antioxidant defense are improved by overexpressing or functionally modifying IMM potassium channels and calcium transporters. Additionally, drug resistance is facilitated by increased mitophagy and anti-apoptotic proteins that inhibit m-PTP opening. This review discusses the functions of mitochondrial ion channels.

RevDate: 2026-01-23
CmpDate: 2026-01-23

Yuan K, Dai T, Gao X, et al (2026)

Mitochondrial heterogeneity drives the evolution of fungicide resistance in Phytophthora sojae, with associated fitness trade-offs.

Science advances, 12(4):eadz4601.

Mitochondrial complex III inhibitors, such as ametoctradin, are crucial for controlling oomycete diseases. However, the increasing severity of fungicide resistance necessitates urgent clarification of its evolutionary mechanisms to optimize disease management and delay resistance development. The DddA-derived cytosine base editors (DdCBEs)-mediated base editing in oomycetes confirmed that the PsCytb[S33L] mutation is sufficient to confer ametoctradin resistance in Phytophthora sojae. We clarified that low-resistant and medium-resistant mutants serve as transitional populations during the resistance evolution process, with high-resistant mutants eventually becoming the dominant population. We revealed the dynamic changes in mitochondrial heterogeneity under fungicide selection, proving that the gradual increase of mutated mitochondria drives resistance evolution. There is a trade-off between ametoctradin resistance and fitness. While the PsCytb[S33L] mutation confers this resistance, it impairs mitochondrial function and thereby reduces fitness. Up-regulation of TFAM1, however, can partially offset this fitness cost. Resistance evolution in plant pathogens involves not only standing variation but also de novo mutations, providing unique insights into the "chicken-and-egg" dilemma.

RevDate: 2026-01-22
CmpDate: 2026-01-22

Hu H, He L, Chen R, et al (2026)

Genome-wide identification and multi-dimensional functional characterization of the SIR2 family in Brassica napus L.

PloS one, 21(1):e0340688.

Silent Information Regulator 2 (SIR2) family proteins are NAD+-dependent histone deacetylases that play key roles in epigenetic regulation, plant development, and stress responses; however, systematic characterization of this family (hereafter SRTs) in the important oilseed crop Brassica napus (rapeseed) remains limited. In this study, we identified 4 SRT genes in the rapeseed genome, designated BnaASRT1/2 and BnaCSRT1/2, based on their homology to Arabidopsis SRTs and chromosomal localization. These genes encode proteins with conserved SIR2 domains, sharing >80% sequence identity and >95% coverage with Arabidopsis SRTs, and exhibit similar subcellular localizations (SRT1s in the nucleus, SRT2s in mitochondria). Phylogenetic and synteny analyses confirmed the evolutionary conservation of rapeseed SRTs, which originated from whole-genome duplication events and were stably inherited from its diploid ancestors (Brassica rapa and Brassica oleracea). Structural analysis indicates that gene structure, motifs, and promoter elements related to stress and hormone responses are conserved, although subtle differences in the promoters suggest functional specialization. Notably, GO enrichment and molecular docking assays demonstrated that BnaSRTs possess histone deacetylase activity, with strong binding affinity to key acetylation sites (e.g., H3K9ac). Treatment with the SIRT-specific inhibitor nicotinamide (NAM) significantly elevated histone acetylation levels and altered the expression of genes involved in photosynthesis, metabolism, and stress responses-further supporting BnaSRTs' ole in epigenetic regulation. Furthermore, expression profiling via the BnIR database showed tissue-specific expression of BnaSRTs (e.g., high BnaASRT2 expression in buds, flowers, and siliques) and dynamic responses to abiotic stresses (salt, drought, cold) and hormones (ABA, JA, IAA), with BnaSRT2s showing the most prominent expression changes. Collectively, these findings clarify the evolutionary conservation, structural features, and functional roles of the SIR2 family in rapeseed, laying a foundation for epigenetic improvement of its agronomic traits.

RevDate: 2026-01-21

Huang X, Zhao L, Liu Z, et al (2026)

ATG5-HSP90.2-mediated micromitophagy as a cytological basis for maternal inheritance of plant mitochondria.

Nature plants [Epub ahead of print].

Mitochondria are inherited maternally in most plants as a classical paradigm of non-Mendelian inheritance, but the mechanism underlying paternal mitochondrial elimination (PME) remains almost unknown. We report here that angiosperms have evolved micromitophagy-mediated PME, in which vacuoles directly engulf paternal mitochondria via tonoplast invagination. We show that micromitophagy occurs specifically in male germline (MG) cells. To gain mechanistic insights, we used a vegetative-to-germline cell fate transition system to establish that micromitophagy is triggered by MG cell fate determination. We found evidence that ATG5 is translocated to vacuoles upon MG-cell-fate determination and interacts with mitochondrion-located HSP90.2 during mitochondrial engulfment by vacuoles, elucidating a cell-type-specific ATG neofunctionalization to mediate micromitophagy. This mechanism not only contributes to maternal inheritance of plant mitochondria but also supports the zygote-to-embryo transition. We further determined that micromitophagy is conserved in angiosperms but was continually optimized during evolution to support the best functioning of PME in MG cells with different properties. These findings bridge a long-standing gap in understanding plant PME with emerging mechanistic knowledge.

RevDate: 2026-01-21
CmpDate: 2026-01-21

Nehela Y, N Killiny (2026)

Not just a cycle: mitochondrial CsgabD is involved in GABA metabolism during citrus defense against biotic stress.

Plant molecular biology, 116(1):11.

While the role of succinic semialdehyde (SSA) dehydrogenase (SSADH; also known as gabD) is well-reported from model plants, the lack of functionality and structure of SSADH from citrus represents a significant knowledge gap. Herein, genome-wide analyses identified 17 high-confidence SSADH-like proteins from Citrus sinensis, among which three putative SSADHs have potential GABA dehydrogenase function. Sequence alignment, phylogenetic analyses, and domain architecture demonstrated high conservation among CsSSADHs (aka CsgabD) and their homologs across diverse plant taxa. Notably, CsSSADH-2 lacked a conserved QGIVC motif found in CsSSADH-1/-3. Secondary structure analyses indicated conserved aldehyde dehydrogenase domains. Homology-based 3D modeling predicted CsSSADH-1 and 2 as homo-tetramers; however, AlphaFold2-based modeling suggested their full-length monomer structures. PPI networks revealed CsSSADH-1 interacts with 10 proteins, primarily involved in GABA/succinate metabolism and the TCA cycle. Docking studies indicated that CsSSADH-1 displayed acceptable affinity and binding modes with GABA, SSA, and succinate. GABA supplementation enhances CsSSADH expression, GABA, and succinate content in a dose-dependent manner in both healthy and infected citrus plants under greenhouse conditions. CsSSADH was involved in citrus responses to 'Candidatus Liberibacter asiaticus' and/or its vector, Diaphorina citri. Nevertheless, GABA accumulation under biotic stress leads to condition-specific rerouting of GABA metabolism. Chemical inhibition of CsSSADH resulted in increased GABA accumulation but reduced succinate levels in both healthy and infected plants. This study offers the first comprehensive characterization of C. sinensis SSADH isoforms, providing insights into their evolutionary divergence, structural features, and potential functions, and enhancing our understanding of their possible roles in GABA metabolism and citrus defense responses.

RevDate: 2026-01-21
CmpDate: 2026-01-21

Wu S, Bakky MAH, Zhang M, et al (2026)

Harnessing mitochondrial quality control in oxidative stress and environmental resilience in aquaculture.

Veterinary research communications, 50(2):121.

Mitochondria, as central hubs of cellular metabolism and signaling, play a pivotal role in mediating the physiological response of aquatic animals to environmental stressors, largely through their involvement in oxidative stress pathway and quality control mechanism. Understanding these molecular pathways is crucial for addressing key challenges in both aquaculture and environmental toxicology. Rather than focusing on the established fact of stress induced mitochondrial damage, this review synthesizes current knowledge to highlighting the emerging role of the mitochondrial quality control (MQC) system as a decisive determinant of stress resilience. A key research evolution is documented, showing a shift from describing oxidative stress towards exploiting MQC for adaptation and performance optimization. Furthermore, a novel theoretical framework is proposed, explaining how aquatic animals perceive and respond to environmental stress through a multi-stage process: 'stress perception-metabolic reprogramming-quality control'. This framework not only integrates a wide range of existing research but also pinpoints key intervention points for enhancing stress resilience. Collectively, these findings provide a significant theoretical foundation and practical guidance for stress tolerance breeding in aquaculture, precise environmental management, and sustainable development.

RevDate: 2026-01-19

Zhong Y, Zhang J, Jia A, et al (2026)

Three-ringed mitochondrial architecture and inter-compartmental gene exchange reveal dynamic genome evolution in Durio zibethinus (Malvaceae).

International journal of biological macromolecules pii:S0141-8130(26)00285-0 [Epub ahead of print].

Durian (Durio zibethinus), often hailed as the "king of fruits", is a tropical tree of high economic and nutritional value whose mitochondrial genome has remained virtually unexplored. Here, we report the first complete mitochondrial genome sequences of durian, assembled from two cultivars 'Monthong' and 'Kanyao'. Both assemblies revealed a striking three-ringed multipartite structure totaling 2.27 Mb, representing the largest and most structurally complex mitogenomes reported to date in Malvaceae. These circular subgenomes are interconnected by numerous repeat sequences that mediate frequent recombination and dynamic structural interconversion. Comparative and evolutionary analyses uncovered extensive bidirectional DNA transfer among the mitochondrial, chloroplast, and nuclear genomes, positioning durian mitochondria as a hub of inter-compartmental gene exchange. Evolutionary rate analyses revealed that most shared organellar genes are under strong purifying selection, whereas a subset-including rps4 and atp1 exhibits signatures of adaptive evolution, suggesting fine-tuned coadaptation between the nucleus and mitochondria. Moreover, durian's mitochondrial genome is exceptionally repeat-rich: comparative mitogenomics across 25 Malvaceae species identified short repeats (30-500 bp) as major drivers of genome expansion in this lineage. Together, these findings not only fill a major gap in durian genomics but also advance our understanding of how repeat-driven structural variation and nuclear-cytoplasmic gene flux shape mitochondrial genome evolution.

RevDate: 2026-01-18

Meguro-Horike M, Iwata K, Matsuzaki H, et al (2026)

Haploinsufficiency of MBD5 and MBD6 impairs mitochondrial respiration through chromatin-mediated gene regulation.

Biochemical and biophysical research communications, 800:153288 pii:S0006-291X(26)00051-3 [Epub ahead of print].

Autism spectrum disorder (ASD) is a highly heritable neurodevelopmental disorder, yet the molecular mechanisms linking ASD-associated genes to cellular dysfunction remain incompletely understood. Among methyl-CpG binding domain (MBD) proteins, MBD5 and MBD6 are recurrently disrupted in individuals with ASD, but their roles in neuronal cells remain poorly defined. Here, we investigated the cellular and transcriptional consequences of MBD5 and MBD6 haploinsufficiency using human neuroblastoma SH-SY5Y cells. We established MBD5-and MBD6-heterozygous SH-SY5Y cell lines by genome editing and performed genome-wide transcriptome analysis. Microarray profiling revealed widespread transcriptional dysregulation characterized by predominant gene upregulation, consistent with repressive roles for both proteins. Notably, a shared subset of downregulated genes was enriched for mitochondrial-related functions, including COX17, COX4I2, DHRS2, MCUB, and PDK1. These expression changes were validated by quantitative real-time PCR. Analysis of publicly available ChIP-seq datasets further demonstrated co-localization of MBD5, MBD6, and components of the BAP1 complex at the COX17 promoter, suggesting direct chromatin-mediated regulation. Functionally, MBD5 and MBD6 haploinsufficiency impaired mitochondrial respiration, as evidenced by reduced basal and ATP-linked oxygen consumption rates without changes in mitochondrial content. Consistent with this defect, heterozygous cells exhibited severe growth impairment under galactose conditions and a compensatory shift toward glycolytic metabolism. Together, these findings uncover a previously unrecognized chromatin-mitochondria regulatory axis linking MBD5 and MBD6 haploinsufficiency to mitochondrial dysfunction, providing mechanistic insight into how epigenetic dysregulation may contribute to ASD pathogenesis.

RevDate: 2026-01-18
CmpDate: 2026-01-18

Gabas ML, Otvos LP, Almeida NBO, et al (2026)

Design-driven optimization of mitochondrial protein phosphatases for in vitro studies.

Biochemical and biophysical research communications, 799:153200.

Molecular cloning and heterologous protein expression are essential for investigating protein function and interactions with ligands such as small molecules, drugs, and other proteins. Studies on the redox regulation, intermolecular interactions, structural determination, and structural dynamics of mitochondrial protein phosphatases require high-yield expression of soluble, catalytically active enzymes. Accordingly, the aim of this study was to optimize the cloning, expression, and soluble purification of mitochondrial protein phosphatases in their monomeric and active forms. We designed 22 expression constructs encoding the mitochondrial protein phosphatases PTPMT1, PP2Cm, PPTc7, and PGAM5, incorporating variations with or without the mitochondrial targeting sequence (MTS) and solubility-enhancing fusion tags. Our results demonstrate that, for matrix localized phosphatases, MTS removal combined with a soluble fusion tag is essential for obtaining soluble, structurally stable, properly folded, and catalytically active proteins. In contrast, intermembrane space phosphatase PGAM5 was well structured and active across constructs, thoug MTS presence reduced expression yields and increased protein instability. Overall, this work underscores the critical role of rational construct design for the successful production of mitochondrial protein phosphatases suitable for in vitro biochemical and structural studies.

RevDate: 2026-01-16
CmpDate: 2026-01-16

Liang L, Feng Y, Han Z, et al (2026)

Comparative analysis of mitochondrial genomes and evolutionary characteristics of five Alternaria species causing potato leaf spot diseases.

Fungal biology, 130(1):101715.

Mitochondria play a central role in fungal metabolism, adaptation, and pathogenesis, yet the evolutionary dynamics of mitochondrial genomes in plant-pathogenic Alternaria species remain poorly understood. In this study, we conducted a comprehensive comparative mitochondrial genomes analysis of five economically important Alternaria species-Alternaria burnsii, A. tenuissima, A. arborescens, A. alternata, and A. gossypina-to investigate structural architecture, genomic variation, selection pressures, repeat element dynamics, and phylogenetic relationships. The mitochondrial genomes exhibited a conserved gene content of 13-14 core genes, 30-33 tRNA and 2 rRNA, but varied in size due to differences in intron insertions, intergenic spacers, and repetitive sequences. Strong A/U-biased codon usage was observed across species, consistent with high AT-richness and translational optimization. Purifying selection dominated across essential respiratory complexes (cox1-3, atp6-9 and cob), indicating functional constraint, while signals of positive selection and pseudogenization (disrupted rps3 in A. burnsii YUN-Z1107) suggest lineage-specific adaptations. We identified evolutionary hotspots in both coding and non-coding regions enriched with InDeLs and repeat expansions. A total of 920 simple sequence repeats (SSRs) were annotated, with A. burnsii YUN-Z1107 showing the highest SSR density, particularly pentanucleotide motifs, implicating replication slippage in genome plasticity. Long repetitive elements were associated with intron mobility and possible recombination events, especially in A. arborescens YUN-Z0872. Phylogenomic analysis of 29 Ascomycota species confirmed a monophyletic Alternaria clade within Pleosporales, although limited resolution within the genus suggests complex evolutionary histories. Our findings support a "conserved core with flexible periphery" model of mitochondrial genomes evolution, where mitochondrial innovation contributes to host adaptation and pathogenicity. This study highlights the mitochondrial genomes as an active driver of fungal evolution and provides a foundation for exploring mitochondria-host coevolution in plant-pathogen interactions.

RevDate: 2026-01-14
CmpDate: 2026-01-14

Ahrendt SR, Haridas S, Stong S, et al (2026)

Comparative mitogenomics of kingdom Fungi - evolutionary insights and metagenomic applications.

Nucleic acids research, 54(2):.

Mitochondria are essential components of eukaryotic cells, responsible for ATP production through oxidative phosphorylation. Despite their biological importance, unique challenges have hindered the adoption of automated mitochondrial genome (mitogenome) annotation methods, obstructing mitochondrial comparative genomics in a broad evolutionary context. Using Fungi as a study system and a Joint Genome Institute (JGI) annotated high-quality reference set, we observed broad patterns of mitochondrial evolution across the kingdom. We found that the median fungal mitogenome size is 58 kb and identified exceptionally large examples over 1 Mb in Pezizomycetes. All 14 expected oxidative phosphorylation protein-coding genes, plus rps3, were generally conserved. We found evidence of major evolutionary transitions within the Ascomycota, including the transfer of mitochondrially encoded atp8 and atp9 to the nuclear genomes across the Pezizomycotina and shifts in mitogenome tRNA patterns across the kingdom. We found substantial concordance between mitochondrial and nuclear evolution, enabling us to document 3131 total fungal mitogenomes from JGI-derived metagenomic datasets. We also identified 6467 total undeclared mitogenomes embedded in Genbank fungal nuclear assemblies. We provide interactive tools for mitogenome analysis through the JGI MycoCosm platform. Collectively, this work generated nearly 10 000 new fungal mitogenome annotations, providing a foundation and resources for future exploration of comparative fungal mitogenomics.

RevDate: 2026-01-14
CmpDate: 2026-01-14

Feng C, Ren X, Xing T, et al (2026)

Bimodal Visualization of Mitochondrial Viscosity Remodeling, Morphological Dynamics and Interorganelle Networks in Acute Kidney Injury.

Analytical chemistry, 98(1):354-363.

The spatiotemporal dynamics of mitochondrial viscosity and its regulatory relationship with organelle interaction networks in cisplatin-induced acute kidney injury (AKI) remain poorly understood, primarily due to the absence of high-precision, multiscale, cross-modal imaging technologies. To overcome this limitation, we pioneered a "trinity" molecular probe design strategy that synergistically integrates electrostatic-driven organelle targeting, microenvironment viscosity-responsive activation, and fluorescence-photoacoustic signal coamplification. Based on this paradigm, we developed ACP, an intelligent dual-modal probe that enables functional spatiotemporal mapping of mitochondrial viscosity dynamics in cisplatin-injured HK-2 cells. Furthermore, we established a sophisticated multiparameter quantitative analysis framework, combining dihedral angle spatial conformation analysis, nanometer-scale organelle membrane distance measurement, and mitochondrial morphometry to systematically decode the dynamic evolution of mitochondrial-lysosomal interaction networks during AKI progression. Therefore, the molecular probe technology and multimodal analytical framework developed in this study may open new avenues for AKI research and pave the way for deeper understanding of organelle-level pathophysiology.

RevDate: 2026-01-13
CmpDate: 2026-01-13

Punia V, Das G, Kumar S, et al (2026)

Comparative diagnostic performance of microscopy and PCR assays with preliminary mitochondrial sequence analysis of Babesia species infecting dogs in Jabalpur, central India.

Molecular biology reports, 53(1):286.

BACKGROUND: The present study evaluated the diagnostic performance of conventional microscopy and polymerase chain reaction (PCR) based assays for the detection of Babesia infections in dogs, including semi-nested PCR (SN-PCR) targeting the 18 S rRNA gene and single-round PCR (SR-PCR) assays targeting the mitochondrial cytochrome b (cytb) and cytochrome c oxidase subunit 1 (cox1) genes for B. gibsoni and B. vogeli, respectively. Mitochondrial sequence variation was further assessed by integrating newly generated sequences from Jabalpur, Madhya Pradesh (central India), with global reference datasets.

METHODS AND RESULTS: A total of 100 blood samples from dogs suspected of having haemoprotozoan infections were analysed between June 2022 and May 2023. Microscopic examination of Giemsa-stained smears detected Babesia parasites in 13% of the samples, whereas the 18 S rRNA SN-PCR assay identified infections in 29%, comprising B. gibsoni (25%) and B. vogeli (4%). Representative sequences showed 98-99% identity with corresponding GenBank reference sequences. Representative sequences showed 98-99% identity with corresponding GenBank reference sequences. Compared with SN-PCR, microscopy demonstrated moderate sensitivity but perfect specificity, resulting in an overall diagnostic accuracy of 84.0% (p < 0.01). Mitochondrial SR-PCR assays detected B. gibsoni and B. vogeli in 5% and 4% of the samples, respectively. The cytb-based assay showed higher sensitivity and a significant diagnostic association (p < 0.01) than the cox1 assay, whereas the cox1 assay demonstrated lower sensitivity with a non-significant association (p > 0.05). All PCR assays showed 100% specificity and positive predictive value. Bayesian phylogenetic and haplotype analyses indicated that B. gibsoni cytb sequences formed a monophyletic lineage with limited regional structuring, with Indian isolates clustering within a distinct sub-lineage. In contrast, B. vogeli cox1 sequences exhibited low global diversity with a dominant shared haplotype across geographic regions.

CONCLUSIONS: The 18S rRNA SN-PCR assay showed the highest sensitive method for detecting Babesia infections in dogs. Mitochondrial markers (cytb and cox1) supported species confirmation and comparative phylogenetic assessment, highlighting the complementary value of nuclear and mitochondrial gene targets for molecular surveillance and control of canine babesiosis in India.

RevDate: 2026-01-13
CmpDate: 2026-01-13

Yilmaz A, OE Kasap (2025)

Prevalence of Wolbachia in natural sand fly (diptera: psychodidae) populations from Türkiye and its potential role in mitochondrial divergence.

Parasites & vectors, 19(1):16.

BACKGROUND: Phlebotomine sand flies are vectors of various pathogens, most notably Leishmania spp. Symbiotic bacteria have recently gained considerable attention owing to their effects on hosts and on other organisms co-infecting the same host. In this study, we investigated the natural Wolbachia infection status of sand fly taxa distributed in Türkiye and examined its potential role in driving the deep mitochondrial divergence observed within certain taxa.

METHODS: We analysed 858 sand fly specimens, mostly collected between 2005 and 2016, with additional samples obtained in 2023. Specimens were morphologically identified, and the mitochondrial cox1 gene was sequenced for DNA barcoding. For selected taxa showing marked mitochondrial divergence, species delimitation methods were applied, and genetic diversity indices and neutrality tests were calculated. Wolbachia infection was detected via PCR amplification of the wsp gene, and strain diversity was characterised using multilocus sequence typing (MLST) of five housekeeping genes. Logistic regression was used to evaluate associations between infection status and mitochondrial lineage, sex or collection period.

RESULTS: Wolbachia infection was detected in 16.67% of specimens, occurring exclusively in Phlebotomus papatasi, Ph. major s.l., Ph. tobbi, Ph. economidesi and Sergentomyia minuta. Analyses of wsp and MLST data identified all sequences as belonging to Supergroup A, with multiple strains present within and across host taxa. Infection among the five Ph. major s.l. lineages delineated by species delimitation was significantly associated with lineage, with lineages 3-5 showing a higher probability of infection. The reduced haplotype and nucleotide diversity, along with a significant negative deviation from neutrality observed in lineage 5, suggest a selective sweep likely driven by Wolbachia infection.

CONCLUSIONS: This study represents the first comprehensive screening of Wolbachia infection in sand fly taxa distributed across Türkiye, during which several novel Wolbachia strains were identified. Our findings suggest a potential role of Wolbachia infection in driving lineage differentiation within certain sand fly taxa. However, further detailed investigations are required to elucidate the mechanisms by which Wolbachia influences sand fly diversification and to assess the broader epidemiological implications related to sand fly-borne diseases (SFBDs).

RevDate: 2026-01-11
CmpDate: 2026-01-11

Dong Y, Li G, Zhang Y, et al (2026)

Gluconolactonase SMP30 deletion worsens fungal degeneration through ROS accumulation and mitochondrial dysfunction in an insect fungal pathogen.

Pest management science, 82(2):1912-1920.

BACKGROUND: Gluconolactonase/Senescence marker protein 30 (SMP30) is a multifunctional enzyme involved in L-ascorbic acid biosynthesis, ROS scavenging, and aging in mammals, but its role in fungi remains partially understood.

RESULTS: Here, we demonstrate that an SMP30 (MrSMP30-1) from the entomopathogenic fungus Metarhizium robertsii is essential for ROS elimination and mitochondrial function. Phylogenetic analysis shows that MrSMP30-1 is more closely related to SMP30 proteins from phytopathogenic fungi than to those from other entomopathogens. Recombinant MrSMP30-1 displays maximum lactonase activity at pH 6.5 and 25 °C. Deletion of MrSMP30-1 results in intracellular ROS buildup, a significant decrease in lipid droplets, and collapse of mitochondrial membrane potential, leading to accelerated, spontaneous fungal degeneration. Virulence tests indicate that the loss of MrSMP30-1 reduces pathogenicity. Immunoprecipitation combined with mass spectrometry identified seven proteins, including polyketide synthase 3, that potentially interact physically with MrSMP30-1.

CONCLUSION: Our results indicate that the gluconolactonase MrSMP30-1 is essential for ROS detoxification and preserving mitochondrial integrity in M. robertsii. This not only enhances our understanding of SMP30's proposed role in fungi but also suggests that it could serve as a biomarker for monitoring fungal culture degeneration. © 2025 Society of Chemical Industry.

RevDate: 2026-01-10
CmpDate: 2026-01-10

Zhan Q, Tang Y, Zhao Y, et al (2025)

Complete Mitochondrial Genome Sequencing of Brachypelma albiceps and Comparative Codon Usage Bias Analysis Across Seven Mygalomorphae Species.

Biology, 15(1): pii:biology15010016.

Tarantulas (family Theraphosidae) are ecologically significant invertebrate predators in terrestrial ecosystems, but many species face threats from habitat fragmentation and unsustainable collection for the international pet trade. Brachypelma albiceps, a CITES Appendix II-listed species, lacks comprehensive mitochondrial genome characterization, limiting phylogenetic and evolutionary studies. Here, we report a complete mitochondrial genome sequence for B. albiceps (13,856 bp; GC content 32.84%) and provide detailed annotation. The genome exhibits typical metazoan mitochondrial organization, containing 13 protein-coding genes (PCGs), 22 tRNAs, and 2 rRNAs, with an AT-rich nucleotide composition (67.16%) characteristic of arthropod mitochondria. Comparative analyses of B. albiceps and six other Mygalomorphae species revealed strong biases toward A/T-ending codons and avoidance of G/C-ending codons. ENC-GC3s, neutrality, and PR2 analyses consistently indicate that natural selection plays a dominant role in shaping synonymous codon usage, with mutation pressure also contributing. Phylogenetic reconstruction based on 10 high-quality mitochondrial protein-coding genes from 23 spider species confirmed the placement of B. albiceps within the family Theraphosidae and its close phylogenetic relationship to Cyriopagopus species. These results provide valuable genomic resources for the Theraphosidae systematics, enhance our understanding of codon bias evolution, and provide critical DNA barcode data for forensic identification of CITES-regulated specimens in the illegal wildlife trade.

RevDate: 2026-01-07
CmpDate: 2026-01-07

Melrose J (2026)

Roles for Electrochemical Proton Gradients in Mitochondrial Energy Production and Neurosensory Processes in Health and Disease.

Developmental neurobiology, 86(1):e70006.

This study reviews the roles of proton electrochemical gradients in ubiquitous mitochondrial energy production systems in cellular activation and functions in neurosensory signaling. Proton electrochemical gradients crucially shaped the evolution of life. The emergence of the proton-motive force in mitochondria was fundamental in energy production and central to the function of eukaryotic cells. Dysfunctional mitochondria, however, result in impaired formation of proton gradients and a wide spectrum of diseases. This is particularly prominent in tissues with high energetic demands, such as muscle and nervous tissues. Oxidant stress generated by dysfunctional proton conductance in the brain results in Alzheimer's and Parkinson's disease, muscular sclerosis, amyotrophic sclerosis, and Huntington's disease. In these disorders, oxidative stress, protein misfolding, and neuroinflammation lead to dysfunctional neuronal activity, neuronal damage, and death. Advancements in nanozyme-engineered synthetic enzymes offer a promising innovative approach to the treatment of these disorders. Nanozymes target proton conductance and the oxidant species they generate, scavenging oxygen free radicals and restoring redox balance, and offer neuronal protection and functional recovery of brain tissues. Neural injury and associated neurological diseases affect almost 1 billion people globally, so there is a clear need to develop effective methods that stimulate neural repair and regeneration. Glycosaminoglycans with proton capture and transport properties regulate intercellular signaling processes, synaptic functions, and cellular communication. Electroconductive hydrogels are showing impressive results in neural repair and regeneration. Glycosaminoglycans, particularly keratan sulfate, show useful electroconductive proton capture and transport properties, suggesting they may be worth evaluation in such procedures.

RevDate: 2026-01-07
CmpDate: 2026-01-07

Wang JJ, Ng PLP, Powers ME, et al (2026)

The role of mitotype variation and positive epistasis in trait differences between Saccharomyces species.

Genetics, 232(1):.

Many traits of interest in biology evolved long ago and are fixed in a particular species, distinguishing it from other sister taxa. Elucidating the mechanisms underlying such divergences across reproductive barriers has been a key challenge for evolutionary biologists. The yeast Saccharomyces cerevisiae is unique among its relatives for its ability to thrive at high temperature. The genetic determinants of the trait remain incompletely understood, and we sought to understand the role in its architecture of species variation in mitochondrial DNA. We used mitochondrial transgenesis to show that S. cerevisiae mitotypes were sufficient for a partial boost to thermotolerance and respiration in the Saccharomyces paradoxus background. These mitochondrial alleles worked best when the background also harbored a pro-thermotolerance nuclear genotype, attesting to positive epistasis between the two genomes. The benefits of S. cerevisiae alleles in terms of respiration and growth at high temperature came at the cost of worse performance in cooler conditions. Together, our results establish this system as a case in which mitoalleles drive fitness benefits in a manner compatible with, and fostered by, the nuclear genome.

RevDate: 2026-01-06
CmpDate: 2026-01-06

Talarico L, Petrosino G, Rossi AR, et al (2025)

Efficient eDNA-based assessment of mitochondrial lineage diversity in wild brown trout populations.

Scientific reports, 16(1):317.

Among the numerous applications of environmental DNA (eDNA), the assessment of genetic diversity in wild populations of target taxa remains moderately investigated. Focusing on 10 selected sites inhabited by brown trout (Salmo trutta complex) in central Italian watercourses, we: (1) developed a non-invasive genetic monitoring protocol combining environmental DNA sampling, amplicon sequencing with custom-designed primers targeting a 192 bp fragment of the mitochondrial Control Region (CR) - whose evolutionary lineages are informative for brown trout phylogeography and genetic conservation status-and a curated reference database; (2) validate it comparing CR lineages assemblages revealed by eDNA with those obtained through traditional CR genotyping of trouts collected by electrofishing in recent surveys, while accounting for uncertainty associated with sample size of genotyped individuals. The two methods returned strongly correlated per-site raw frequencies of CR lineages (Pearson r = 0.93, p < 0.0001), and remarkably similar lineage assemblages (Mantel r = 0.832, p = 0.0001). Concordances between (semi-quantitative) lineage assemblages retrieved by the two methods increased at increasing trout densities and decreased at warmer water temperatures. Discordances mostly involved low-frequency lineages that were not detected by traditional CR genotyping. This study supports the effectiveness of eDNA for reliably characterising mitochondrial intra-population diversity in brown trout, a widely distributed and actively managed taxon of important conservation and economic value, offering a valuable tool to assist the genetic monitoring of wild populations, including the identification and quantification of exotic lineages.

RevDate: 2026-01-05
CmpDate: 2026-01-05

Lee S, Chakraborty S, Kim S, et al (2025)

Organelles harbour pH gradients.

bioRxiv : the preprint server for biology.

Organelle pH is critical to organelle identity and function. Resident proteins that define each organelle modify transiting cargo proteins, with both retention and trafficking between organelles governed by pH-dependent mechanisms. For example, lysosomal enzymes bind mannose-6-phosphate receptors at the higher pH (~6.5) of the Golgi and dissociate at the lower pH (~5.5) of late endosomes[1]. Proteins that stray from the endoplasmic reticulum (ER) are captured by KDEL receptors in the acidic Golgi and returned into the neutral ER[2,3]. This pH-tuned trafficking system compartmentalizes organelle function and prevents mis-localization of critical enzymes[4]. Dysregulated organelle pH disrupts their function and leads to various diseases. Because protons move rapidly in water, the pH within a single organelle is currently assumed to be spatially uniform[5]. Here, using a reporter sensitive from pH 5.5 - 10.5 to map a spectrum of organelles at high resolution, we discovered that pH gradients exist within single, large or long organelles such as the ER and mitochondria, and in membrane-less organelles without ion-transporting proteins such as the nucleolus. These new findings upend our understanding of organellar pH, prompting new questions about proton diffusion within the cell, and its potential consequences on organelle function.

RevDate: 2026-01-02
CmpDate: 2026-01-02

Lu Z, Xia R, Xu A, et al (2025)

Oxygen-adaptive plasticity of Asgard archaea dependent on terminal oxidase and globin.

bioRxiv : the preprint server for biology pii:2025.11.07.685452.

The oxygenation of ancient Earth is thought to have driven eukaryogenesis, beginning with the endosymbiosis of an aerobic alphaproteobacterium (proto-mitochondria) with an archaeal host. Given that the archaeal host likely evolved from within Asgard archaea (phylum Promethearchaeota), the metabolic traits of Asgard archaea could provide key insights into eukaryotic origins. Although Asgard archaea cultured to date are obligate anaerobes, their genomes encode oxygen-adaptive proteins, suggesting they might be oxygen-tolerant. Here, we demonstrate that some Asgard archaea, in particular, Hodarchaeales , the closest known relatives of eukaryotes, and Kariarchaeaceae , exhibit oxygen adaptation mediated by terminal oxidase and globin. Phylogenetic analysis reveals long-term vertical evolution of terminal oxidases in Asgard archaea, suggesting ancient adaptation to molecular oxygen. By contrast, globin was likely acquired by Asgard archaea via horizontal gene transfer from facultative aerobic Chloroflexales bacteria. Heterologous expression of the Asgard globin enhances aerobic growth of Haloarchaea and Escherichia coli in the presence of terminal oxidase-dependent electron transfer chain, suggesting that Asgard growth benefits from ambient oxygen. The Asgard globin gene is embedded in an oxygen-sensitive bidirectional promoter region, with one promoter driving oxygen-induced globin expression, and the other anaerobically activating expression of two enzymes, PdxS and PdxT, involved in a pyridoxal 5'-phosphate biosynthesis. The Asgard globin and promoter region exhibit high functional robustness across archaea and bacteria, and could contribute to the symbiosis between the Asgard and aerobic bacterial partners. These findings highlight the oxygen-adaptive plasticity of Asgard archaea and its potential contribution to eukaryogenesis.

RevDate: 2025-12-31
CmpDate: 2025-12-31

Dimogkioka AR, D Rapaport (2025)

Conserved function, divergent evolution: mitochondrial outer membrane insertases across eukaryotes.

Biological chemistry, 406(10-12):423-429.

Mitochondrial function relies heavily on the proper targeting and insertion of nuclear-encoded proteins into the outer mitochondrial membrane (OMM), a process mediated by specialised biogenesis factors known as insertases. These insertases are essential for the membrane integration of α-helical OMM proteins, which contain one or multiple hydrophobic transmembrane segments. While the general mechanisms of mitochondrial protein import are well established, recent research has shed light on the diversity and evolutionary conservation of OMM insertases across eukaryotic lineages. In Saccharomyces cerevisiae, the mitochondrial import (MIM) complex, composed of Mim1 and Mim2, facilitates the integration of various α-helical OMM proteins, often in cooperation with import receptors such as Tom20 and Tom70. In Trypanosoma brucei, the functional MIM counterpart pATOM36 performs a similar role despite lacking sequence and structural homology, reflecting a case of convergent evolution. In mammals, MTCH2 has emerged as the principal OMM insertase, with MTCH1 playing a secondary, partially redundant role. This review provides a comparative analysis of these insertases, emphasising their conserved functionality, species-specific adaptations, and mechanistic nuances.

RevDate: 2025-12-30
CmpDate: 2025-12-30

Wu Y, Xu J, Hong T, et al (2025)

The Complete Mitochondrial Genome of Callicarpa americana L. Reveals the Structural Evolution and Size Differences in Lamiaceae.

Biology, 14(12): pii:biology14121747.

Callicarpa americana L. is a member of the Lamiaceae family with important ornamental and medicinal value. Although the chloroplast genome of Lamiaceae has been extensively studied, its mitochondrial genome remains unreported, limiting a comprehensive understanding of the phylogeny and genome evolution of Lamiaceae. In this study, the complete mitochondrial genome of C. americana was successfully assembled for the first time. The genome is 499,565 bp in length, showing a complex multi-branched closed-loop structure that contains 37 protein-coding genes, 23 tRNA genes, and 4 rRNA genes. The difference in mitochondrial genome size is relatively large compared to Orobanchaceae species, but the difference in GC content is not obvious. The expansion of genome size was mainly due to the accumulation of non-coding regions and repetitive sequences. Meanwhile, two pairs of long repetitive sequences (LR3 and LR5) mediated homologous recombination. The mitogenome was also identified; there were a total of 494 C-to-U RNA editing sites in protein-coding genes. In addition, 42 mitochondrial plastid DNA fragments (MTPTs) were detected, with a total length of 21,464 bp, accounting for 4.30% of the genome. Repeat sequence analysis showed that tetranucleotide SSR was the most abundant repeat type in the mitochondria of Lamiaceae. Phylogenetic analysis based on the alignment of 32 protein-coding gene sequences showed that Callicarpa is sister to the other eight species of Lamiaceae. This work fills an important gap by presenting the first complete mitochondrial genome of C. americana, providing an important data resource for further understanding the structural evolution, dynamic recombination mechanism, and phylogeny of the mitochondrial genome of Lamiaceae.

RevDate: 2025-12-30
CmpDate: 2025-12-30

Sun YT, WX Yang (2025)

Gatekeepers of the Germ Line: How Mitochondria Shape Reproductive Evolution in Metazoans.

Biology, 14(12): pii:biology14121728.

Mitochondria play essential roles for animal reproduction, influencing not only cellular energetics but also gamete quality, inheritance and evolutionary patterns. Currently, most research still focuses on chordates or mitochondrial diseases and their impact on the health of germ cells. However, few studies focus on integrative synthesis that connect comparative morphology, inheritance mechanisms and evolutionary theory. In this review, we integrate cross-phyla evidence to explore two interconnected dimensions: the fate of mitochondria during gametogenesis and the strategy shaping their evolution. We compare mitochondrial morphology, distribution, and metabolic strategies in gametogenesis, revealing how these traits align with reproductive modes and ecological adaptations. Then we further discuss how mitochondrial genome evolution, bottleneck effects and mito-nuclear coevolution contribute to germline stability and maternal inheritance. Special attention is given to exceptional systems such as Doubly Uniparental Inheritance (DUI) in bivalves, which challenges conventional mode of strictly maternal transmission and illuminates the flexibility of mito-nuclear evolution. Altogether, these perspectives highlight mitochondria as gatekeepers and evolutionary recorders in the reproductive systems across metazoans, providing a unifying framework for future research across ecology, evolution and molecular biology.

RevDate: 2025-12-30
CmpDate: 2025-12-30

Xie V, Franco MC, LJ Martin (2025)

Human Mutant Dynactin Subunit 1 Causes Profound Motor Neuron Disease Consistent with Possible Mechanisms Involving Axonopathy, Mitochondriopathy, Protein Nitration, and T-Cell-Mediated Cytolysis.

Biomolecules, 15(12): pii:biom15121637.

Mutations in the gene encoding the p150 subunit of the dynactin complex (DCTN1) are linked to amyotrophic lateral sclerosis, spinal and bulbar muscular atrophy, and Perry syndrome. These neurodegenerative diseases can cause muscle weakness and atrophy, parkinsonian-like symptoms, and paralysis. To examine the evolution of neuropathology caused by a mutation in DCTN1 and cellular mechanisms of disease for therapeutic discovery, we characterized mice expressing either human wildtype or mutant (G59S) DCTN1. Neuron-specific expression of mutant, but not wildtype, DCTN1 caused fatal age-related paralytic disease and motor neuron (MN) degeneration in the spinal cord with axonopathy and chromatolysis without apoptotic morphology. MNs became positive for cleaved caspase-3, cleaved caspase-8, and nitrated Hsp90. Mitochondria accumulated and appeared fragmented and dysmorphic and then were lost. This pathology was accompanied by invasion of CD95- and CD8-positive mononuclear T cells into the ventral horn and accumulation of TNFα and IL9. Administration of the mitochondrial division inhibitor-1 (Mdivi-1) protected MNs and extended the lifespan of G59S-DCTN1 mice. A mitochondrial permeability transition pore inhibitor also extended lifespan. Thus, mutant DCTN1 causes degeneration of MNs associated with axonopathy, mitochondriopathy, nitrative stress, and caspase activation. It appears as retrograde neurodegeneration and inflammatory T-cell-like cytolysis. Mitochondria are possible therapeutic targets in DCTN1-linked neurodegenerative disorders.

RevDate: 2025-12-26
CmpDate: 2025-12-26

Muravyov G, DA Knorre (2025)

Mechanisms of Intracellular Selection of Mitochondrial DNA.

Biochemistry. Biokhimiia, 90(12):1919-1928.

Eukaryotic cells contain multiple mitochondrial DNA (mtDNA) molecules. Heteroplasmy is coexistence in the same cell of different mtDNA variants competing for cellular resources required for their replication. Here, we review documented cases of emergence and spread of selfish mtDNA (i.e., mtDNA that has a selective advantage in a cell but decreases cell fitness) in eukaryotic species, from humans to baker's yeast. The review discusses hypothetical mechanisms enabling preferential proliferation of certain mtDNA variants in heteroplasmy. We propose that selfish mtDNAs have significantly influenced the evolution of eukaryotes and may be responsible for the emergence of uniparental inheritance and constraints on the mtDNA copy number in germline cells.

RevDate: 2025-12-26
CmpDate: 2025-12-26

Belosludtsev KN, Dubinin MV, NV Belosludtseva (2025)

Ca[2+]-Dependent Mitochondrial Permeability Transition Pore: Structure, Properties, and Role in Cellular Pathophysiology.

Biochemistry. Biokhimiia, 90(12):1789-1810.

The Mitochondrial Permeability Transition pore (MPT pore) activated by Ca[2+] ions is a phenomenon that has long been the subject of intense study. Cyclophilin D-dependent opening of the MPT pore in mitochondria in response to calcium overload and oxidative stress leads to swelling of the mitochondrial matrix, depolarization of the inner membrane and dysregulation of ion homeostasis. These processes are accompanied by damage to mitochondrial membranes and, ultimately, to cell death. Despite decades of research, the molecular identity of the MPT pore remains unclear. Currently, the inner membrane proteins - ATP synthase and adenine nucleotide translocator (ANT) - are considered to be its key structural components, along with the regulatory protein cyclophilin D. The involvement of the MPT pore in the progression of various pathological conditions and diseases, as well as in a number of physiological processes, such as the regulation of cellular bioenergetics and rapid release of Ca[2+], is widely discussed. This review summarizes modern molecular genetic data on the putative structure of the MPT pore, traces the evolution of views on its functioning - from interpreting it as a simple experimental artifact to its recognition as a putative key regulator of energy metabolism - and also considers the mechanisms of its regulation and its multifaceted pathophysiological role.

RevDate: 2025-12-23

Nuryadi H, Anoop VK, Kakioka R, et al (2025)

Routine mitochondrial recombination drives rapid concerted evolution of duplicated control regions in a wild fish.

Heredity [Epub ahead of print].

Duplications and concerted evolution of control regions (CRs) in animal mitogenomes have been reported across diverse taxa, yet the tempo and mechanism of gene conversion remain poorly understood. Here, we assembled the complete mitochondrial genome of the western Indian ricefish Oryzias setnai and found that the CR is duplicated. Comparative analysis of CR1 and CR2 sequences across individuals sampled throughout the species' range revealed that they are identical in most individuals, and differ by only one or two mutations in the rest-indicating recent and ongoing concerted evolution. We estimated that gene conversion events occur at a rapid pace, on the order of once every 1000 years or less. Using both short- and long-read amplicon sequencing, we directly detected a substantial number of recombinant mitogenome molecules resulting from homologous recombination between CR paralogues. This provides the first clear evidence that homologous recombination is the mechanism driving mitochondrial gene conversion. Our findings challenge the prevailing view that recombination in animal mitochondria is exceedingly rare, and demonstrate that mitogenome recombination can occur routinely in natural populations.

RevDate: 2025-12-23

Yuan F, Li W, Li A, et al (2025)

Mitochondrial remodeling and metabolic reprogramming drive long-term salinity adaptation in Tetrahymena thermophila.

mSystems [Epub ahead of print].

Salinization of inland waters, driven by climate change and human activities, poses a major threat to aquatic ecosystems. While species can swiftly adapt to environmental stress, the molecular mechanisms underpinning this adaptation remain to be fully elucidated. This study seeks to clarify the complex adaptive strategies employed by the freshwater ciliate Tetrahymena thermophila in response to chronic salt stress through the methodologies of experimental evolution and multi-omics integration. The findings indicate that three lineages adapted to salt (ST-4, ST-8, and ST-12), which evolved under a regime of increasing NaCl concentration, demonstrated a trade-off between delayed growth and osmotic resilience. Transcriptomic and proteomic analyses revealed key evolutionary priorities, including (i) the co-upregulation of pathways related to DNA replication, glutathione metabolism, and endoplasmic reticulum (ER) protein processing, (ii) the suppression of lipid catabolism alongside the accumulation of lipid droplets mediated by START2, and (iii) mitochondrial remodeling through the expansion of ER contacts to sustain ATP production. Interestingly, the adaptation to salt appears to tolerate genome instability induced by replication stress through the dysregulation of replisome components, specifically the upregulation of Prim1 and downregulation of LIG, while also evading antioxidant defenses via the compartmentalization of oxidative damage. These results contribute to a framework in which protists effectively balance lipid-mediated osmoregulation, controlled mutagenesis, and organelle metabolism to navigate salinity challenges, thereby offering predictive insights into microbial adaptation thresholds within evolving ecosystems.IMPORTANCESalinization of inland waters is a growing concern due to climate change and human activities. Understanding how organisms adapt to saline environments is vital. Tetrahymena thermophila, a model organism, was studied to explore its adaptation mechanisms. The findings show that through gene regulation, it can acclimate to high salt conditions. The role of mitochondria in metabolic reprogramming during this process is significant. This research contributes to a more profound understanding of how organisms adapt to saline stress and the molecular mechanisms underlying such adaptations, which may aid in predicting and managing the impacts of salinization on aquatic ecosystems.

RevDate: 2025-12-20

Si R, Shen Z, Sui Y, et al (2025)

Suppressing the OTUD7A/KDM5B/GABPA axis enhances the sensitivity of cisplatin through inducing ferroptosis in KRAS-mutant LUAD.

Cell death & disease pii:10.1038/s41419-025-08337-x [Epub ahead of print].

KRAS-mutant lung adenocarcinoma (LUAD), due to its evolution of more complex antioxidant metabolic mechanisms, exhibits poorer sensitivity to conventional platinum-based drugs compared to other types of LUAD. Ferroptosis, as a means of inducing cell death in cancer therapy, shows unique features and potential therapeutic effects compared to the conventional form of apoptosis, which is frequently obstructed by drug resistance. In human KRAS-mutant LUAD cell lines and mouse models, we found that the deubiquitinase OTU deubiquitinase 7A (OTUD7A) precisely regulates the lysine demethylase 5B (KDM5B). Inhibition of KDM5B expression increases the H4K20me3 level, which in turn downregulates the expression of transcription factor GABPA associated with mitochondrial function, ultimately promoting the production of more Reactive Oxygen Species (ROS) by mitochondria and inducing ferroptosis. Additionally, in in vivo organoid models, cisplatin (CDDP) induced ferroptosis combined with GABPA inhibition demonstrated superior anticancer effects compared to conventional platinum-based drugs. This research identifies new targets and regulatory networks that hold promise for developing ferroptosis-based therapies for KRAS-mutant LUAD.

RevDate: 2025-12-17
CmpDate: 2025-12-17

Kuznetsov P, E Temereva (2025)

Toward the Origin and Evolution of Unique Echiurid Excretory Organs: New Data From Females of Bonellia viridis.

Journal of morphology, 286(12):e70105.

Echiurids, as nonsegmented annelids, have an excretory system of a special organization. The excretory system of the echiuran worms is known to consist of ultrafiltration zones on blood vessels and anal sacs. Prior to this study, the fine structure of the anal sacs had been described in detail only for Thalassema thalassemum (Thalassematinae). In contrast, the more complex anal sacs of Bonelliinae, which contain additional structural elements such as tubules, remained unexplored. This study describes the anatomy, histology, and ultrastructure of the anal sacs of Bonellia viridis Rolando, 1822 (Bonelliinae) using a set of modern morphological methods: computer microtomography, araldite histology, scanning and transmission electron microscopy. New data suggest functional implications for structural elements of the anal sacs: the conical part and the neck of the funnel, the tubules, and the end sac. The ciliary funnels are responsible for collecting filtrate to their conical parts and can close at their base, thus preventing reverse flow. According to the ultrastructural data, the inner epithelium of the tubules and the end sac modifies the incoming filtrate in two ways. The inner epithelium of the tubules carries out pinocytosis and accumulates electron-dense granules. The inner epithelium of the end sac has a basal labyrinth consisting of basal processes with numerous mitochondria extending deep into the extracellular matrix and indicates active ion transport. Additional zones responsible for ultrafiltration were identified in the outer epithelium of the anal sac-specifically within the tubule and at the base of the funnel. The origin of the echiurid anal sacs as a result of fusion and multiplication of the metanephridia at the posterior growth zone of metameric annelid-like ancestor is suggested.

RevDate: 2025-12-11
CmpDate: 2025-12-11

Valencia-Montoya WA, Liénard MA, Rosser N, et al (2025)

Infrared radiation is an ancient pollination signal.

Science (New York, N.Y.), 390(6778):1164-1170.

Color and scent are well-known pollinator cues. Some plants also produce heat, but its role remains unclear. Here, we report that plant-generated thermal infrared radiation serves as a pollination signal and describe the underlying mechanisms of heat production and infrared detection. Mitochondrial adaptations heat plant reproductive structures in a circadian pattern, radiating infrared that is sufficient to attract beetle pollinators. Beetle antennae contain infrared-activated neurons with thermosensitive ion channels that are structurally tuned to match host plant thermogenesis. Comparative analyses revealed that infrared is among the earliest pollination signals, and indicate a deep-time transition from infrared-based to color-dominated signaling in flowering plants. Our findings uncover an ancient sensory modality shaping the early evolution of pollination, one of the world's most vital processes linking plants and animals.

RevDate: 2025-12-13
CmpDate: 2025-12-10

Nguyen THM, Klein DA, Weklar OS, et al (2025)

Abundant Recurrent Mitochondrial Mutations and Widespread Mitonuclear Epistasis in Caenorhabditis elegans.

Molecular biology and evolution, 42(12):.

Coordinated genetic and physical interactions between mitochondrial and nuclear gene products regulate ATP production in the mitochondria. Linking mitochondrial genotypes and mitonuclear genetic interactions to phenotypes remains a complex challenge. Here, we have developed Caenorhabditis elegans as a model for mitonuclear epistasis studies. In a sample of 540 genetically distinct wild isolates, 10% of sites in the mitochondrial genome vary, with hundreds of missense mutations segregating in the species. Recurrent mutations and triallelic sites are common. Phylogenetic analyses of mitogenome sequences identified 8 distinct lineages, each with diagnostic variants. Principal component analysis of the nuclear genomes showed considerable concordance between mitochondrial and nuclear genomes in C. elegans populations, suggesting that disrupting coevolved mitonuclear genetic combinations could reveal substantial epistasis. We used GPR-1 overexpression, which disrupts the first mitotic division, to efficiently exchange nuclear and mitochondrial genomes between all pairs of 18 naturally isolated C. elegans strains, generating the largest-to-date animal mitonuclear exchange panel, with 323 unique viable mitonuclear genotypes. We phenotyped development of a subset of strains, with 30 unique genotypes, under 6 different environmental conditions, including high temperature and exposure to heavy metals. Mitonuclear epistasis contributed significantly to phenotypic variance across all tested conditions. We also tested for mitonuclear coadaptation by comparing the stress resistance of matched and mismatched cybrids. Interestingly, some mismatched strains exhibited greater resistance, highlighting the complexity and context dependence of mitonuclear interactions.

RevDate: 2025-12-08

Luangtrakul W, Söderhäll K, I Söderhäll (2025)

The role of mitophagy during hematopoiesis in an invertebrate, Pacifastacus leniusculus.

Journal of immunology (Baltimore, Md. : 1950) pii:8374194 [Epub ahead of print].

Freshwater crayfish as most aquatic crustaceans live for up to 20-30 years on the bottom of lakes and rivers, constantly exposed to millions of microorganisms. Consequently, they must have an effective immune system to combat and eliminate pathogens. The main immune cells are the hemocytes, and they are regularly consumed during the animal's whole life and are continuously produced through hematopoiesis. We used DMSO as a tool to induce differentiation of hematopoietic stem cells and we can show that differentiation of hematopoietic stem cells to mature hemocytes in a freshwater crayfish is preceded by degradation of mitochondria by mitophagy and this process could be inhibited by a mitophagy inhibitor. The differentiation process was regulated by β-catenin signaling in similarity to differentiation of human neutrophils. A better understanding of the molecular mechanisms that regulate hemocyte development in these animals will provide new insights into the evolution of the innate immune system and hematopoiesis in general.

RevDate: 2025-12-07
CmpDate: 2025-12-07

Okamoto T, Okamoto K, Yamamoto T, et al (2025)

A mitogenomic phylogenetic analysis of the Japanese Plestiodon species (Scincidae, Squamata) clarifies a mito-nuclear discordance caused by a past long distance dispersal.

Genetica, 154(1):3.

The whole mitochondrial genomes (mitogenomes) excluding the control region were sequenced for 42 samples of the ten species of scincid lizards of the genus Plestiodon occurring in Japan, and the mitochondrial genealogy of the East Asian Plestiodon was reconstructed on the basis of the mitogenomic dataset. A comparison with a species phylogeny based on five nuclear DNA fragments revealed that P. latiscutatus, a species distributed on the Izu Peninsula of the Japanese Main Islands, was a sister to the clade consisting of P. japonicus and P. finitimus, species occurring in the remaining parts of the Main Island in the species phylogeny, whereas the former species was a sister to the P. capito group occurring in continental China in the mitogenomic phylogeny. A tree reconciliation analysis of the species and the mitochondrial phylogenies revealed horizontal transfer of mitochondria, suggesting that the position of P. latiscutatus was caused by past introgression of mtDNA from the ancestral P. capito group to the ancestral P. latiscutatus. This further suggests a past long-distance dispersal of the skink from the Eurasian continent to the Izu Peninsula and Izu Islands beyond the western part of the Japanese Main Islands in the Miocene.

RevDate: 2025-12-05

Pham NT, Duplouy A, See J, et al (2025)

A high-quality draft genome assembly of the Neotropical butterfly, Batesia hypochlora (Nymphalidae: Biblidinae).

BMC genomics pii:10.1186/s12864-025-12394-z [Epub ahead of print].

We report a long-read high-coverage reference genome assembly of the Neotropical butterfly, Batesia hypochlora (Nymphalidae: Biblidinae). This represents the first reference genome in the Biblidinae subfamily, a clade subject to ongoing studies on seasonal and climate adaptation in the Amazon. We assembled the genome from PacBio HiFi long reads (66X coverage), polished it with Illumina short reads (15X coverage), and annotated it using PacBio IsoSeq RNA data. We observed 15 chromosome-sized scaffolds, varying in length from 13.2 Mbp to 37.6 Mbp (median, 24.3 Mbp), which combined to form a total genome size of 395.788 Mbp. This assembly is highly contiguous (contig N50 of 25.14 Mbp) and complete (BUSCO completeness score of 98.6% and 0.2% duplication rate). Repeat annotation revealed that the genome comprises approximately one-third transposable elements. Gene prediction using RNA-seq evidence identified 19,395 genes, of which 17,400 were assigned to 2,883 orthogroups, including genomes of the fruit fly, silk moth, and three other Nymphalid butterfly species. The high sequencing depth also allowed us to assemble the genomes of the mitochondria and the common endosymbiotic bacterium Wolbachia. The mitochondrial genome was fully assembled (15,540 bp in size) with all expected genes annotated. The Wolbachia genome was fragmented, and we determined that it belongs to the B-supergroup. The high-quality assembly of B. hypochlora can represent the subfamily in further comparative analysis of evolution and provide a key resource for ongoing work to explore reproductive biology and adaptations to seasonality in Neotropical butterflies.

RevDate: 2025-12-19
CmpDate: 2025-12-19

Yu X, Li M, H Li (2025)

The role of gut dysbiosis and mitochondrial dysfunction in type 2 diabetes: Insights on pathogenesis, intervention and future perspective.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 193:118846.

Type 2 diabetes (T2D) is a typical metabolic disease which is attributed to genetic and environmental factors. Emerging evidence has highlighted that either gut dysbiosis or mitochondrial dysfunction plays critical roles in the development of T2D through various ways. After searching preclinical and clinical studies, our review concludes that gut dysbiosis contribute to T2D through gut metabolites-induced inflammation, dysregulation of glucose homeostasis and the change of β-cell evolution. Moreover, we found out that the overproduction of oxidative stress, disruption of energy metabolism, mitochondrial dynamic network and mitochondrial permeability transition are major mechanisms which contribute to the development of T2D by mitochondrial dysfunction. We particularly focused on summarizing the advances of how gut dysbiosis and mitochondrial dysfunction contributed to T2D development, respectively, and elaborating their interplay in central and peripheral organs. Moreover, the latest strategies on T2D management were also discussed, in which modulation on gut microbiota and mitochondrial function were primarily included, as well as perspectives on future investigations.

RevDate: 2025-12-03

Ramanathan S, Hanraths A, Xie J, et al (2025)

Plant organelle C-to-U RNA editing factors can operate successfully in yeast (Saccharomyces cerevisiae) as an easily amenable eukaryotic system for their functional analysis.

The FEBS journal [Epub ahead of print].

Site-specific cytidine-to-uridine (C-to-U) RNA editing is essential for gene expression in plant mitochondria and chloroplasts. Specific RNA-binding pentatricopeptide repeat (PPR) proteins equipped with a DYW-type cytidine deaminase have been identified as the core RNA editing factors. Multiple circumstances impede their analysis in planta and call for experimental approaches in easily amenable heterologous setups for functional analyses of these intriguing proteins. Here, we report the establishment of the yeast Saccharomyces cerevisiae as such a system. Three plant RNA editing factors from the model moss Physcomitrium patens, namely PPR56 (PpPPR_56), PPR65 (PpPPR_65), and PPR78 (PpPPR_78), were successfully expressed in the yeast cytosol and faithfully edit not only their respective co-delivered targets but also variable ranges of off-targets with similar recognition sequences in the yeast background transcriptome. Convincingly, we found that the different editing factors behaved in the new system very much like previously found in bacteria or human cells, not only with respect to off-target conservation profiles but also with surprising differences in off-target numbers, championed by more than 125 off-targets for PPR56 with editing efficiencies of up to 41% in the S. cerevisiae transcriptome. We conclude that S. cerevisiae will be a helpful heterologous system for studying the intricacies of plant RNA editing.

RevDate: 2025-11-30
CmpDate: 2025-11-27

Jeon M, Yang SS, Lee S, et al (2025)

From Congenital Torticollis to Leigh Syndrome: A Case Report of Diagnostic Evolution in an Infant.

Children (Basel, Switzerland), 12(11):.

Leigh syndrome is a rare, progressive mitochondrial disorder of childhood. Early diagnosis is often challenging due to nonspecific clinical manifestations. We report a 1-month-old male infant initially referred for suspected congenital muscular torticollis who ultimately received a diagnosis of Leigh syndrome. Despite unremarkable perinatal history, he subsequently developed persistent feeding difficulties, recurrent vomiting, failure to thrive, and global developmental delay. Early neurological assessment revealed poor repertoire patterns on General Movement Assessment. The Neonatal Oral-Motor Assessment Scale (NOMAS) demonstrated dysfunctional oral-motor control, whereas the video fluoroscopic swallowing study (VFSS) revealed aspiration during swallowing. Brain MRI revealed symmetric basal ganglia lesions. Expanded whole-exome sequencing identified a pathogenic MT-ATP6 m.8993T>G variant with high heteroplasmy level (>90% in blood), confirming the diagnosis of Leigh syndrome. The variant was maternally inherited, although neither the mother nor the older sibling exhibited clinical features of mitochondrial disease. Leigh syndrome can initially manifest with subtle systemic features rather than overt neurological features. Persistent feeding difficulties and growth delay in infancy warrant thorough evaluation, including neuroimaging and comprehensive genomic testing, to enable timely diagnosis and optimize clinical management.

RevDate: 2025-11-27

Iannello M, Piccinini G, Salatiello F, et al (2025)

New insights into mitochondrial segregation from the Doubly Uniparental Inheritance system in bivalves.

BMC biology pii:10.1186/s12915-025-02459-6 [Epub ahead of print].

BACKGROUND: While nuclear genome segregation is well characterized, mechanisms underlying mitochondrial partitioning remain partially obscure, even though its failure can cause developmental arrest or harmful mutations. This knowledge gap invokes the need for new, more suitable model systems to study such mechanisms. Doubly Uniparental Inheritance (DUI) of mitochondria in bivalves is a useful system for such studies. In DUI, sperm mitochondria in male embryos are actively transported across cell divisions to precursors of the germline, and this male-specific pattern depends on maternal factors stored in eggs. The presence of distinct mitochondrial segregation patterns in male and female embryos offers a unique opportunity to investigate the molecular bases of this process.

RESULTS: Here, we leveraged this system by (1) performing RNA-Seq on eggs producing male-biased versus female-biased progenies in the Mediterranean mussel Mytilus galloprovincialis to identify factors involved in differential mitochondrial segregation; and (2) inferring signatures of convergent evolutionary rate across DUI bivalve genomes to separate segregation-specific factors from those involved in sex determination. We show that differentially transcribed genes across eggs that give rise to either male- or female-biased progeny are predominantly associated with mitochondrial dynamics, cytoskeletal organization, and vesicular trafficking. We also identified multiple long noncoding RNAs-many derived from transposable elements-that might have roles in the regulation of other maternally supplied factors that shepherd paternal mitochondria.

CONCLUSIONS: By overlaying clues from expression and sequence evolution, we delineate a conserved protein-protein interaction network of factors that mediate mitochondrial segregation. This study reveals general principles of organelle selection in animals and unveils the contribution of new factors.

RevDate: 2025-11-28
CmpDate: 2025-11-25

Kim G, Choi EH, UW Hwang (2025)

Three distinct genetic lineages of Trichonephila clavata based on mitochondrial COI and genome-wide SNPs on the Korean Peninsula.

Scientific reports, 15(1):41911.

Trichonephila clavata L. Koch, 1878, an East Asian species renowned for its long-distance ballooning dispersal, has recently drawn attention as an invasive species following its introduction into the southeastern United States. However, few population genetic studies have been undertaken to investigate population genetic diversity and structure which will be helpful for its management. Here, we examined ten populations of T. clavata on the Korean Peninsula using mitochondrial COI and genome-wide SNP data to broadens the understanding of genetic and demographic processes of the species. Our results revealed: (1) high genetic diversity in COI but relatively low diversity in SNPs; (2) the presence of three genetic lineages detected by both markers; (4) population expansion in each COI genetic lineage and constant population size in each SNP genetic lineage; and (5) stepwise lineage divergence estimated based on COI and lineage divergence with admixture event based on SNPs. These findings suggest that multiple factors, which are ballooning dispersal, demographic dynamics and geological event, may play a pivotal role in shaping population genetic patterns with geographic co-occurrence among the lineages. Consequently, this study provides insights into the genetic architecture of natural populations and offers a valuable baseline for understanding the population genetic pools of invasive populations of this species.

RevDate: 2025-11-25

Montalvo RN (2025)

Postmodern Mitochondria and The Architecture of Function.

RevDate: 2025-11-28
CmpDate: 2025-11-25

Mingoti GZ, Nunes GB, Souza-Cáceres MB, et al (2025)

Extracellular Vesicles Derived From Antral Follicles Significantly Change the Transcriptional Profile of Cumulus Cells and Oocytes During Pre-In Vitro Maturation in Cattle.

Molecular reproduction and development, 92(11):e70068.

Cumulus-oocyte complexes (COCs) used for in vitro production (IVP) of bovine embryos originate from antral follicles of different sizes, leading to variations in developmental competence. To address this, pre-in vitro maturation (pre-IVM) allows oocytes with additional time to acquire developmental competence. Given the role of follicular fluid-derived extracellular vesicles (EVs) in ovarian follicle communication, which has been shown to vary in content and function across folliculogenesis, we investigated whether EVs from early versus late antral follicles influence COCs during pre-IVM. EV supplementation significantly altered gene expression in cumulus cells and oocytes. In cumulus cells, affected pathways included MAPK signaling, Gap junctions, Cytokine-cytokine receptor interaction, Axon guidance, cAMP, and Cushing syndrome. In oocytes, fewer genes were altered, with effects on Inositol phosphate metabolism, p53 signaling and Cholesterol metabolism. Despite these changes, no significant effects of the EV treatment were noted on oocyte chromatin configuration and developmental competence, except for a significant increase of mitochondrial membrane potential (Δψm) in blastocysts. In conclusion, EV supplementation during pre-IVM significantly altered the transcriptional profile of COCs, with EVs from early follicles modulating the expression of genes regulating cumulus cell proliferation and gap junctions, while EVs from late follicles impacted pathways associated with meiotic resumption, cumulus cell expansion, and apoptosis. Along with improved Δψm in blastocysts, these results support a positive effect of EVs on bovine COCs, but further research is needed to better characterize the functional consequences, mainly in terms of the effects of early versus late follicle-derived EVs on oocyte developmental potential.

RevDate: 2025-11-26
CmpDate: 2025-11-24

Wang X, Guo Z, Tao J, et al (2025)

Phylogeny and comparative analysis of mitochondrial genomes of Gomphus spp. Pers. (Basidiomycota, Agaricomycetes), with descriptions of G. matijun J.W. Liu & F.Q. Yu and G. bijiensis sp. nov.

MycoKeys, 124:357-381.

The genus Gomphus Pers. presents persistent taxonomic challenges due to its morphological similarities with related genera. In this study, we collected two specimens of Gomphus from Guizhou, China; one specimen is described as a new species, Gomphus bijiensis sp. nov. and the other is identified as G. matijun J.W. Liu & F.Q. Yu based on morphological traits and phylogenetic analyses of the nuclear rDNA internal transcribed spacer (ITS) and nuclear rDNA large subunit (LSU). To resolve their evolutionary relationships we assembled and annotated the mitochondrial genomes of both species using next-generation sequencing. Comparative analyses revealed codon usage strongly biased toward A- or U-ending codons, consistent with the low GC content typical of fungal mitochondria. Variation in protein-coding gene lengths and base composition suggests that diverse evolutionary pressures have shaped these genomes. Divergence time estimation indicates that morphological diversity within Gomphus and related macrofungi has largely resulted from convergent evolution. Phylogenetic reconstruction places G. bijiensis and G. matijun within a distinct clade, supporting their close evolutionary affinity and the coexistence of ancestral and derived traits. This study provides the first comprehensive mitochondrial genomic data for Gomphus, offering new insights into its taxonomy, phylogeny, and evolutionary dynamics, and establishing a framework for future studies within the Gomphaceae.

RevDate: 2025-11-26
CmpDate: 2025-11-24

Shan S, Qing Y, Chen S, et al (2025)

Characterization of the complete mitochondrial genome data of Asiatic Toad, Bufo gargarizans (Cantor, 1842) (Neobatrachia: Bufonidae) from Mianyang, China.

Data in brief, 63:112213.

A common amphibian in East Asia, the Bufo gargarizans is significant for research on ecology, conservation biology, and evolution. Thus, the B. gargarizans mitochondrial genome was sequenced and subjected to a methodical analysis. The sequence was 17,431 base pairs long, with 13 protein-coding genes (PCG), 22 transfer RNA (tRNA) genes, 2 ribosomal RNA (rRNA) genes, and a D-loop control region. The nucleotide base composition of the mitochondrial genome was skewed toward AT content (57.17%), including adenine (28.80%), thymine (28.37%), cytosine (27.40%), and guanine (15.43%). For phylogenetic analysis, Bayesian inference (BI) techniques were used to build a phylogenetic tree from the mitochondrial genomes of 27 other species and the B. gargarizans. The findings demonstrated that species of the Bufonidae family formed a monophyletic group with the B. gargarizans. The mitochondrial genome of B. gargarizans will serve as an invaluable asset for future investigations into the evolution, taxonomy, and genetic preservation strategies of this species. Mitochondria genomic data can be found in GenBank under accession number PV083742.

RevDate: 2025-11-26
CmpDate: 2025-11-22

Bilinski SM, Sekula M, Sochaczewska M, et al (2026)

Analysis of Bush Cricket Oogenesis Provides an Insight into the Function and Anagenesis of an Enigmatic Organelle Assemblage: The Balbiani Body.

Results and problems in cell differentiation, 76:167-182.

Balbiani body (Bb) is an intricate, oocyte-specific organelle complex described in the ooplasm of nearly all examined vertebrates and invertebrates. The Bb is devoid of a limiting membrane and consists of such organelles as elements of endoplasmic reticulum (ER), Golgi complexes (GCs), mitochondria, and characteristic accumulations of fibrillo-granular material, termed the "nuage." Despite numerous studies, the functioning of the Bb remains not completely understood. Until now at least four disparate functions have been attributed to the Bb: (1) delivery of germinal granules and localized mRNAs to the oocyte vegetal cortex; (2) transfer of mitochondria to the polar (germ) plasm; (3) selective elimination of dysfunctional (damaged, containing mutated mitochondrial DNA (mtDNA)) mitochondrial units in female germline cells; and (4) formation of oocyte reserve materials, e.g., lipid droplets. Such functional variability obviously raises several intriguing questions for students of developmental and cellular biology. Here we present the results of our studies on oogenesis of bush crickets that advance our understanding of the Bb function and anagenesis of this organelle complex during the evolution of bilateral animals.

RevDate: 2025-11-20
CmpDate: 2025-11-20

Xie B, Zhang X, Yan M, et al (2025)

Mitogenomic analysis and phylogenetic implications for the Deltocephalinae (Hemiptera: Cicadellidae).

Invertebrate systematics, 39(11):.

Deltocephalinae (Hemiptera: Cicadellidae) is the largest subfamily within the leafhopper family Cicadellidae and has an almost worldwide distribution. However, the classification and phylogenetic relationships of Deltocephalinae have not yet been fully resolved. In this study, we sequenced the complete mitogenomes of 12 Deltocephalinae species and compared them with the 50 previously reported mitogenomes for this subfamily. Mitogenome size ranged from 14,648 bp in Scaphoideus albovittatus to 16,711 bp in Mukaria splendida. All contained 37 genes and a variable number of non-coding A + T-rich regions. Nucleotide composition analysis showed that the AT content was higher than GC. And while most protein-coding genes use ATN as the start codon and TAA or TAG as the stop codons, some genes use T as a stop codon. The Ka/Ks ratio showed that the cox1 gene has the slowest evolutionary rate, while atp8 is the gene with the fastest evolutionary rate. These new analyses confirm that Deltocephalinae mitochondrial genomes are highly conservative in overall structure, with only a few rare rearrangements of tRNAs, primarily concentrated in the trnW-trnC-trnY and trnA-trnR-trnN-trnS1-trnE-trnF gene clusters. Deltocephalinae mitochondrial genomes exhibit gene overlaps with three stable regions: trnW and trnC, atp6 and atp8, nad4 and nad4l. The overlapping sequences are typically AAGTCTTA, ATGATAA and TTATCAT. Phylogenetic analyses by maximum likelihood and Bayesian inference were conducted based on five datasets including either amino acid sequences alone or nucleotide sequences from different combinations of protein coding and ribosomal RNA genes, with or without third codon positions (AA, PCG12, PCG12R, PCG123 and PCG123R). Phylogenies obtained from different analyses consistently supported the monophyly of Deltocephalinae and showed high congruence within the subfamily, with few short, deep internal branches unstable among analyses. Included members of the following tribes were consistently monophyletic: Athysanini, Chiasmini, Deltocephalini, Drabescini, Macrostelini, Paralimnini, Penthimiini, Scaphoideini and Stenometopiini. Consistent with other recent analyses, Fieberiellini, Goniagnathini and Penthimiini are early diverging lineages within Deltocephalinae. Overall, our results indicate that complete mitogenome sequences provide robust data for phylogenetic reconstruction.

RevDate: 2025-11-20
CmpDate: 2025-11-20

Kapan E, Uslu C, Arab H, et al (2025)

Toward Mitochondrial Targeting of Resistant Triple-Negative Breast Cancer Using Triphenylphosphonium-Conjugated Antimicrobial Peptides.

ACS pharmacology & translational science, 8(11):4159-4171.

Metastatic evolution of malignant tumors following standard anticancer therapies and the emergence of resistant cancer cell populations remain major challenges in oncology. One promising strategy is to develop compounds that selectively target mechanisms of therapeutic resistance. Unlike therapy-sensitive malignant cells, which rely primarily on glycolysis for energy, many chemoresistant cells and cancer stem cells (CSCs) preferentially utilize mitochondrial oxidative phosphorylation (OXPHOS). In this study, we employed a triple-negative breast cancer model to demonstrate that short antimicrobial peptides can significantly suppress the metastatic potential of resistant cancer cells and reduce the formation of CSC-like mammospheres by disrupting mitochondrial respiration. This effect was further enhanced by conjugating the peptides to the mitochondrial-targeting cation triphenylphosphonium (TPP). Mechanistic studies revealed that these compounds induce oxidative stress and mitophagy and suppress mitochondrial translation. Collectively, these findings suggest that TPP-conjugated peptides represent a promising therapeutic strategy for targeting OXPHOS-dependent resistance in aggressive solid tumors.

RevDate: 2025-12-10

Valt M, Pánek T, Mirzoyan S, et al (2025)

Rare microbial relict sheds light on an ancient eukaryotic supergroup.

Nature [Epub ahead of print].

During the past decade, our understanding of eukaryotic evolution has increased immensely. Newly recognized eukaryotic supergroups have been established[1-3], and most enigmatic orphan lineages have had their relationships resolved[4-6]. Studies on unicellular protist eukaryotes have also been key to understanding the evolution of mitochondria, the fundamental organelles of the eukaryotic cell, which originated from an alphaproteobacterial ancestor. The retention of ancestral alphaproteobacterial pathways in some protist lineages reveals that the mitochondrion of the last eukaryotic common ancestor was more metabolically versatile than are the highly derived mitochondria that are found in most modern eukaryotes[7,8]. Here we report the discovery of such a unicellular eukaryote, Solarion arienae gen. et sp. nov., an inconspicuous, free-living heterotrophic protist with two morphologically distinct cell types and a novel type of predatory extrusome. We assign Solarion to the new phylum Caelestes. Together with Provora, hemimastigophoreans and Meteora, they form a new eukaryotic supergroup, Disparia. Moreover, S. arienae has some noteworthy traits associated with the mitochondrial genome; in particular, the mitochondrially encoded secA gene, a remnant of an ancestral alphaproteobacterial protein secretion pathway, which has been lost almost entirely in extant mitochondria[9,10]. The discovery of S. arienae broadens our understanding of early eukaryotic evolution and facilitates the study of proto-mitochondrial metabolic remnants, shedding light on the complexity of ancestral eukaryotic life.

RevDate: 2025-11-19
CmpDate: 2025-11-16

Gomes YCP, Bongers A, Jeannin P, et al (2025)

Cerebrospinal Fluid From Patients With HTLV-1-associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) With Rapid Evolution Affects Mitochondrial DNA Transcription and Network Organization in Human Glioblastoma Cells.

Journal of medical virology, 97(11):e70711.

Human T-lymphotropic virus 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a progressive neurodegenerative disease affecting motor and sensory functions. While alterations in cerebrospinal fluid (CSF) have been used to identify disease biomarkers, the effects of such modified CSF on CNS cells remain unexplored. This study compared the effects of pools of CSF from HTLV-1 asymptomatic carriers (HAC) and HAM/TSP patients-categorized by disease progression as: very slow (HAMvs), typical (HAMt), and rapid (HAMr)-on the glioblastoma cell line U87-MG, a cellular model often used to study neurodegenerative diseases. RNA sequencing of U87-MG cells treated with a pool of CSFs from HAMr patients revealed a significant downregulation of transcription of mitochondrial genes after 24 h of treatment. Confocal microscopy showed phenotypical changes in the mitochondrial network: glioblastoma cells exposed to pooled HAMr CSF exhibited a less complex network compared to other patient groups. Despite these changes, U87-MG cells treated with CSF from HTLV-1-infected donors with distinct neurological outcomes presented similar mitochondrial oxygen consumption. In conclusion, these findings show that pooled HAMr CSF induces mitochondrial stress in glioblastoma cells, suggesting that CSF alterations may participate in rapidly progressing HAM/TSP pathogenesis.

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RJR Experience and Expertise

Researcher

Robbins holds BS, MS, and PhD degrees in the life sciences. He served as a tenured faculty member in the Zoology and Biological Science departments at Michigan State University. He is currently exploring the intersection between genomics, microbial ecology, and biodiversity — an area that promises to transform our understanding of the biosphere.

Educator

Robbins has extensive experience in college-level education: At MSU he taught introductory biology, genetics, and population genetics. At JHU, he was an instructor for a special course on biological database design. At FHCRC, he team-taught a graduate-level course on the history of genetics. At Bellevue College he taught medical informatics.

Administrator

Robbins has been involved in science administration at both the federal and the institutional levels. At NSF he was a program officer for database activities in the life sciences, at DOE he was a program officer for information infrastructure in the human genome project. At the Fred Hutchinson Cancer Research Center, he served as a vice president for fifteen years.

Technologist

Robbins has been involved with information technology since writing his first Fortran program as a college student. At NSF he was the first program officer for database activities in the life sciences. At JHU he held an appointment in the CS department and served as director of the informatics core for the Genome Data Base. At the FHCRC he was VP for Information Technology.

Publisher

While still at Michigan State, Robbins started his first publishing venture, founding a small company that addressed the short-run publishing needs of instructors in very large undergraduate classes. For more than 20 years, Robbins has been operating The Electronic Scholarly Publishing Project, a web site dedicated to the digital publishing of critical works in science, especially classical genetics.

Speaker

Robbins is well-known for his speaking abilities and is often called upon to provide keynote or plenary addresses at international meetings. For example, in July, 2012, he gave a well-received keynote address at the Global Biodiversity Informatics Congress, sponsored by GBIF and held in Copenhagen. The slides from that talk can be seen HERE.

Facilitator

Robbins is a skilled meeting facilitator. He prefers a participatory approach, with part of the meeting involving dynamic breakout groups, created by the participants in real time: (1) individuals propose breakout groups; (2) everyone signs up for one (or more) groups; (3) the groups with the most interested parties then meet, with reports from each group presented and discussed in a subsequent plenary session.

Designer

Robbins has been engaged with photography and design since the 1960s, when he worked for a professional photography laboratory. He now prefers digital photography and tools for their precision and reproducibility. He designed his first web site more than 20 years ago and he personally designed and implemented this web site. He engages in graphic design as a hobby.

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In 1994 Bryan Sykes was called in as an expert to examine the frozen remains of a man trapped in glacial ice in northern Italy for over 5000 years―the Ice Man. Sykes succeeded in extracting DNA from the Ice Man, but even more important, writes Science News, was his "ability to directly link that DNA to Europeans living today." In this groundbreaking book, Sykes reveals how the identification of a particular strand of DNA — mitochondrial DNA — that passes unbroken through the maternal line allows scientists to trace our genetic makeup all the way back to prehistoric times―to seven primeval women, the "seven daughters of Eve."

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Collection of publications by R J Robbins

Reprints and preprints of publications, slide presentations, instructional materials, and data compilations written or prepared by Robert Robbins. Most papers deal with computational biology, genome informatics, using information technology to support biomedical research, and related matters.

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Curriculum Vitae for R J Robbins

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