Search Results (184)

Populations of several billfish species are declining due to overfishing and bycatch, and fundamental aspects of their biology and population dynamics remain poorly understood. We provide the first assessment of the population genetic structure of longbill spearfish (Tetrapturus pfluegeri) in the western Atlantic Ocean. We screened variation at 12 nuclear microsatellite loci (n = 144) and mitochondrial DNA control region sequences (mtCR, n = 177). Both marker types revealed three genetically differentiated clusters, with mean values for microsatellites showing differentiation of F_ST = 0.136 and D_EST = 0.201, and for mtCR F_ST = 0.645. Microsatellite markers demonstrated moderate-to-high genetic diversity, with a mean allelic richness of 6.73 alleles per locus, moderate heterozygosities (Ho = 0.446, He = 0.604), and a positive inbreeding coefficient (F_IS = 0.22) across the three sample collection sites. The overall estimated effective population size was 789.2 (95% CI: 246.7–∞). The mtCR exhibited 96 haplotypes, with high haplotype (0.989 ± 0.003) and nucleotide (0.025 ± 1.3%) diversities. We found higher mean relatedness within clusters than among them, supporting the interpretation of population subdivision and the Wahlund effect. Tajima’s D and Fu’s Fs were negative across all localities, with significant values observed along the Brazilian coast but not in the Caribbean Sea. These neutrality test results, together with low Harpending’s raggedness indices from DNA sequence mismatch distributions, are consistent with historical demographic expansion. Our findings establish a genetic baseline for fishery monitoring and management, contributing to the conservation of T. pfluegeri populations in the western Atlantic Ocean. Full article

Lodgepole pine (Pinus contorta Dougl.) exhibits pronounced morphological variation across its range, historically attributed to allopatric differentiation during the Wisconsin glaciation. However, whether genetic divergence aligns with morphological differentiation—a fundamental prediction of allopatric speciation theory—remains untested. We conducted a comprehensive phylogeographic analysis of chloroplast DNA (trnL intron and trnL/trnF spacer) and mitochondrial DNA (nad1 b/c intron) across 31 populations representing all four recognized subspecies to test hypotheses of refugial isolation and to evaluate the genetic basis of current taxonomic classification. Contrary to predictions of allopatric divergence, both organellar genomes showed striking genetic uniformity (π = 0.000178–0.000186; intersubspecific genetic distances: 1.06 × 10⁻⁴ to 3.96 × 10⁻⁴) with no phylogenetic structure corresponding to morphological boundaries. Significant negative neutrality test values (Tajima’s D = −2.26, p < 0.02; Fu and Li’s D* = −4.52, p < 0.02) suggest recent demographic expansion rather than equilibrium divergence. A distinctive 5 bp indel in coastal populations provides molecular evidence for a northern Pacific refugium, and its occurrence in interior populations is consistent with post-glacial pollen-mediated gene flow, though this directionality remains inferential pending nuclear genomic confirmation. These findings suggest that morphological divergence reflects rapid adaptive evolution in heterogeneous environments rather than deep phylogenetic divisions. This pattern exemplifies gene flow-selection balance, in which divergent selection maintains local adaptation despite extensive gene flow—supporting an ecotypic rather than a phylogenetic interpretation of intraspecific diversity. The persistence of morphological variation despite genetic homogeneity indicates strong selection on ecologically important traits, likely driven by variation in fire regimes, differential seed predation, and climate gradients. These results have critical implications for understanding adaptive evolution rates in widespread conifers and for developing conservation strategies that emphasize adaptive processes over taxonomic categories. Full article

Background/Objectives: Cyto-nuclear discordances, resulting from the independent evolutionary histories of cytoplasmic and nuclear genomes, often obscure phylogenetic inference and species delimitation, particularly at shallow taxonomic levels. In this study, we examine the extent and causes of cyto-nuclear discordances within the darkling beetle tribe Akidini (Coleoptera: Tenebrionidae), focusing on the genera Akis Herbst, 1799 and Morica Dejean, 1834. Methods: Using two molecular markers—nuclear histone 3 (H3) and mitochondrial cytochrome c oxidase subunit I (COI)—and a comprehensive sampling from western Europe and northern Africa, we assess reciprocal monophyly, internal relationships, and phylogenetic incongruence across datasets. Results: Discordances between morphological species assignment and mitochondrial topologies may result from retained ancient polymorphisms or historical introgression among closely related species (e.g., Akis genei vs. Akis lusitanica). However, these causes seem less plausible for explaining discordances between nuclear and mitochondrial markers involving non-closely related species (e.g., A. discoidea and A. granulifera). The geographic location of the problematic specimens, limited to a narrow marginal contact zone between the two non-sister species, suggests that local hybridisation may occur. Conclusions: Our results indicate that cyto-nuclear discordances between mitochondrial and nuclear markers, even across morphologically well-differentiated non-sister lineages, may be more frequent than previously assumed in darkling beetles, highlighting both their evolutionary relevance and the need for caution when relying solely on mitochondrial data for species identification. Full article

Recent evidence links lens epithelial cell (LEC) dysfunction and cellular senescence—an irreversible cell cycle arrest with a pro-inflammatory secretory phenotype—to age-related cataract (ARC) progression. This systematic review synthesizes current knowledge on LEC senescence, its molecular features, and laboratory methods for senescence assessment in the ARC. Following PRISMA guidelines, a comprehensive search of PubMed, Scopus and Cochrane databases retrieved 3417 records from inception to 9 February 2025, with 14 studies ultimately included (821 patients and multiple in vitro LEC models). The following multiple senescence expression pathways were identified: SA-β-gal activity, p53/p21 and p16INK4A pathway activation, mitochondrial dysfunction, oxidative stress, and secretion of senescence-associated secretory phenotype (SASP) factors. Notably, cortical cataract demonstrated direct association with local senescent cell accumulation, while nuclear cataract reflected cumulative oxidative damage from impaired LEC-mediated antioxidant defense. Senescence markers correlated positively with cataract severity across multiple studies. Several potential therapeutic targets emerged, including metformin (AMPK activation/autophagic restoration), circMRE11A silencing, NLRP3 inflammasome inhibition, and modulation of FYCO1/PAK1 and MMP2 pathways. This review establishes LEC senescence as a central process in ARC pathogenesis and highlights promising senotherapeutic approaches. Future research should prioritize human surgical samples, develop standardized senescence detection panels (SA-β-gal + p21/p16 + SASP factors), and conduct longitudinal studies to establish causal relationships between senescence accumulation and cataract progression. Full article

Honeybee (Apis mellifera L.) populations are a vital resource for pollination and honey production, yet their genetic diversity in Central Asia remains poorly understood. This study provides a comprehensive genetic assessment of 16 honeybee populations from Kazakhstan, with comparative samples from Russia, Georgia and Kyrgyzstan, utilizing mitochondrial COI–COII intergenic region and 12 highly polymorphic nuclear STR markers. Mitochondrial DNA analysis revealed the predominance of the Eastern European C lineage (A. m. carnica), while a few populations from East Kazakhstan and Russia attributed the M lineage (A. m. mellifera), indicating local introgression and the persistence of relict lineages. STR analyses showed high levels of polymorphism and genetic diversity, with variation in heterozygosity and inbreeding across populations. Analyses of population genetic structure delineated four principal genetic clusters shaped by regional differentiation, historical gene flow, and sporadic admixture. Concordance between mitochondrial and nuclear markers confirms the robustness of these findings. Overall, this study highlights the rich genetic diversity of honeybees from Kazakhstan and emphasizes the importance of conserving local populations and implementing selective breeding programs to sustain adaptive potential and long-term apiculture. Full article

Background: Mitophagy is a critical mitochondrial quality control mechanism that limits neuronal injury following cerebral ischemia/reperfusion injury (CI/RI). Tetramethylpyrazine (TMP), a bioactive alkaloid from Ligusticum chuanxiong Hort., exhibits neuroprotective effects in cerebrovascular disorders. However, whether these effects involve mitophagy regulation remains unclear. Methods: CI/RI was induced using a middle cerebral artery occlusion/reperfusion (MCAO/R) model in mice and an oxygen–glucose deprivation/reoxygenation (OGD/R) model in HT22 cells. Neurological function, infarct volume, mitochondrial function, and mitophagy-related markers were assessed. Pharmacological inhibitors and genetic manipulation of YAP and Parkin were used to investigate underlying mechanisms. Results: TMP treatment significantly reduced infarct volume and improved neurological deficits in MCAO/R mice, accompanied by enhanced mitophagy, as indicated by increased mitochondrial LC3 recruitment and Parkin expression. In OGD/R-injured HT22 cells, TMP promoted mitophagosome and mitolysosome formation, reduced mitochondrial reactive oxygen species, and restored mitochondrial membrane potential. Inhibition of mitophagy with Mdivi-1 attenuated TMP-mediated neuroprotection. Mechanistically, TMP promoted YAP nuclear localization, and inhibition of YAP or silencing of Parkin abolished TMP-induced mitophagy, while Parkin overexpression restored mitophagy under YAP inhibition. Conclusions: TMP alleviates CI/RI by promoting mitophagy through the YAP/Parkin signaling pathway, suggesting mitophagy modulation as a potential therapeutic strategy for ischemic brain injury. Full article

We report a chromosome-level assembly of a male red coachwhip snake (Masticophis flagellum piceus) generated exclusively with nanopore sequencing. Using Hifiasm-ONT for assembly and RagTag for scaffold polishing, we produced a 1.61 Gb nuclear genome comprising 8 macrochromosomes and 10 microchromosomes with a 97.7% BUSCO completeness score. Annotation with LiftOn found 19,832 loci, including 18,025 protein-coding genes. The mitochondrial genome, assembled with MitoHiFi and annotated with MitoFinder, was 17,119 bp with 13 coding genes, 22 tRNAs and 2 rRNAs. All sequencing was performed in a simulated mobile laboratory using a portable sequencer and a laptop with analyses done both locally and remotely. These results highlight the feasibility of decentralized genomics and its potential to accelerate biodiversity research globally. Full article

In the last decades, ozone (O₃)-based medical treatments have become a widely applied complementary therapy for several pathological conditions. O₃ is administered at low dosages since the induction of a mild oxidative stress does not cause damage but stimulates the antioxidant cell response through the nuclear factor erythroid 2-related factor 2 (Nrf2). Mitochondria are sensitive to even mild oxidative stress, thus being a responsive target for O₃. This study aimed to evaluate the mitochondrial response to low O₃ doses used for medical treatments. As the skeletal muscle represents a primary target in local O₃ treatments, a murine non-tumoral muscle cell line was selected as an appropriate in vitro model. Transmission electron microscopy, biochemistry, and flow cytometry provided original information on the O₃ dose-dependent modifications of mitochondrial structural and molecular features. Low O₃ doses promoted an increase in mitochondrial area and in cristae extension, as well as an enhancement of the electron transport chain complexes and of antioxidant catalase and manganese-dependent superoxide dismutase. Nrf2 maintained its association with the outer mitochondrial membrane, thus exerting its protective role. All mitochondrial modifications were observed 24 h after treatment and disappeared after 48 h, demonstrating that cells promptly respond to the O₃-driven oxidative stress, effectively restoring homeostasis. Full article

OGG1 and MUTYH are base excision repair (BER) DNA glycosylases (DGs) from the Helix–hairpin–Helix superfamily responsible for initiating and coordinating the repair of 8-oxo-7,8-dihydroguanine (OG), and its replication-derived mispair with adenine (OG:A), respectively. The DNA repair activities of these DGs are pivotal to safeguarding nuclear and mitochondrial genomes. Indeed, DG functional impairment is associated with numerous pathologies, including neurodegenerative diseases, metabolic syndromes, and cancer. The timely and precise localization and processing of oxidized nucleobases carried out by these DGs are modulated by a complex regulatory network at both transcriptional and posttranslational levels, as well as intricate protein–protein interaction networks. In the absence of regulation, inappropriate and imbalanced DG activity may trigger telomeric instability, changes in transcriptional profiles and cell death. This review focuses on summarizing key features of OGG1 and MUTYH function, with a special emphasis on structure, regulation, and novel emerging roles. Full article

Neurodegenerative diseases (NDs) are the most prevalent age-associated disorders, characterized by progressive neuronal loss and cognitive decline. Mitochondrial dysfunction is strictly associated with NDs and represent one of the hallmarks of these disorders, with neurological syndromes frequently representing the primary clinical manifestations of mitochondrial abnormalities. As central regulators of cellular bioenergetics, mitochondria play a pivotal role in both the physiological maintenance and pathogenesis of disease by different regulatory approaches. One of these, microRNAs (miRNAs), a class of small non-coding RNAs, are well-established regulators of gene expression across different biological pathways. These miRNAs were usually investigated within the cytoplasmic context, but recent discoveries have revealed the presence of these miRNAs in different parts of mitochondria, where they contribute to the regulation of gene expression and metabolic activity. These mitochondrial-localized miRNAs, termed mito-MiRNA, may originate from either nuclear or mitochondrial genomes and have been shown to modulate the translational machinery of the cells. Despite extensive research on cytoplasmic miRNAs, the functional roles of mito-MiRNA remain poorly understood, particularly in the context of neurodegenerative disorders. Based on these findings, this review aims to synthesize emerging evidence on the involvement of mito-MiRNA in in one of most prevalent neurodegenerative diseases—Parkinson’s disease (PD). Full article

Berberine (BBR), a protoberberine alkaloid with a long history of medicinal use, has consistently demonstrated benefits in glucose–lipid metabolism and inflammatory balance across both preclinical and human studies. These diverse effects are not mediated by a single molecular target but by BBR’s capacity to restore network coordination among metabolic, immune, and microbial systems. At the core of this regulation is an AMP-activated Protein Kinase (AMPK)-centered mechanistic hub, integrating signals from insulin and nutrient sensing, Sirtuin 1/3 (SIRT1/3)-mediated mitochondrial adaptation, and inflammatory pathways such as nuclear Factor Kappa-light-chain-enhancer of Activated B cells (NF-κB) and NOD-, LRR- and Pyrin Domain-containing Protein 3 (NLRP3). This hub is dynamically regulated by system-level inputs from the gut, mitochondria, and epigenome, which in turn strengthen intestinal barrier function, reshape microbial and bile-acid metabolites, improve redox balance, and potentially reverse the epigenetic imprint of metabolic stress. These interactions propagate through multi-organ axes, linking the gut, liver, adipose, and vascular systems, thus aligning local metabolic adjustments with systemic homeostasis. Within this framework, BBR functions as a negentropic modulator, reducing metabolic entropy by fostering a coordinated balance among these interconnected systems, thereby restoring physiological order. Combination strategies, such as pairing BBR with metformin, Sodium-Glucose Cotransporter 2 (SGLT2) inhibitors, and agents targeting the microbiome or inflammation, have shown enhanced efficacy and substantial translational potential. Berberine ursodeoxycholate (HTD1801), an ionic-salt derivative of BBR currently in Phase III trials and directly compared with dapagliflozin, exemplifies the therapeutic promise of such approaches. Within the hub–axis paradigm, BBR emerges as a systems-level modulator that recouples energy, immune, and microbial circuits to drive multi-organ remodeling. Full article

Mitochondria not only generate ATP and metabolites essential for nuclear and cytoplasmic processes but also actively shape nuclear epigenetic regulation. Conversely, the nucleus encodes most of the proteins required for mitochondrial functions, and intriguingly, certain nuclear-encoded epigenetic factors—such as DNA and histone modifiers—also localize to mitochondria, where they modulate mitochondria genome stability, gene expression, metabolic flux, and organelle integrity. This reciprocal interplay defines mitochondria as both a source and a target of epigenetic regulation, integrating energy metabolism with gene expression and cellular homeostasis. This review highlights emerging mechanisms that link mitochondrial metabolism to chromatin remodeling, DNA and histone modifications, and transcriptional control, as well as how nuclear epigenetic enzymes translocate into mitochondria and regulates their functions. We also briefly introduce recent methodological advances that enable spatially selective depletion of mitochondrial proteins, offering new tools to dissect this bidirectional communication. Together, these insights underscore mitochondria’s central role as an energetic and epigenetic hub coordinating nuclear function, development, and disease. Full article

Representatives of the family Moinidae (Crustacea: Cladocera) are well-adapted to life in temporary waters. Different species are characteristic of the Arid Belt of Eurasia. We aimed to compare the moinid species composition and genetic diversity found in Djibouti (with extreme and uniform environments) with neighboring Ethiopia (a relatively large country with diverse environmental conditions). Any cladocerans were found in only four localities in Djibouti from Ecoregion 527 (Western Red Sea Drainages) according to Abell et al. (2008). The moinids belonged to two taxa: M. cf. micrura and M. heilongjiangensis. In Ethiopia, moinids were found in 28 water bodies from four other Ecoregions (522, 525, 526 and 528). They belonged to M. micrura and M. belli. A genetic study based on full mitogenomes, sequences of the mitochondrial COI and nuclear ITS1 loci demonstrated that M. micrura from Djibouti and Ethiopia belong to distant lineages. Our genetic analysis revealed a very contrasting moinid fauna in two neighboring countries of the African Horn: there was no single haplotype, clade or even species sharing these territories. We have revealed unexpectedly small genetic distances between Chinese (type locality) and Djiboutian populations of M. heilongjiangensis; the question of the invasive status of the latter could therefore be raised. Moreover, the status of M. micrura populations from the Rift Valley also needs to be checked; they could be non-indigenous, as they belong to “European” M. micrura s. str. Finally, we have demonstrated that M. cf. micrura is not a monophyletic clade. Full article

CYP24A1, a mitochondrial cytochrome P450 enzyme, plays a critical role in the catabolism of active vitamin D metabolites and is a key regulator of local vitamin D signaling in the small intestine. While traditionally studied in the context of renal physiology, increasing evidence highlights its distinct regulatory mechanisms and functional significance within the intestinal epithelium. This review explores the molecular architecture, tissue-specific expression patterns, and multifactorial regulation of CYP24A1 in enterocytes, encompassing nuclear receptor signaling, epigenetic and post-transcriptional control, and environmental influences such as inflammation, diet, and the gut microbiota. We discuss how intestinal CYP24A1 modulates the expression of vitamin D target genes involved in transcellular calcium absorption and epithelial barrier function, and how its dysregulation contributes to gastrointestinal disorders including inflammatory bowel diseases, celiac disease, microbiota dysbiosis, and colorectal cancer. In addition, we examine preclinical and translational evidence supporting CYP24A1 as a potential therapeutic target. Emerging strategies such as selective enzyme inhibitors, microbiota modulation, RNA-based technologies, and personalized supplementation approaches are considered in the context of restoring local vitamin D bioactivity and mineral homeostasis. Together, this review underscores the clinical importance of intestinal CYP24A1 and highlights novel opportunities for targeted interventions in vitamin D-responsive gastrointestinal pathologies. Full article

The Blackspot Seabream, Pagellus bogaraveo, is a commercially valuable species widely distributed in the northeastern Atlantic and Mediterranean. Its biology makes it vulnerable to overfishing, but its population structure and ontogenetic migration strategy remain unclear. Building on previous work based on microsatellite markers, we expanded the investigation by analysing the mitochondrial Control Region (CR) to complement nuclear data. We analysed 199 specimens from 13 sites and combined the new CR sequences with 129 published records to achieve the broadest coverage in terms of biogeographic and genetic data. We calculated genetic diversity and performed AMOVA, pairwise ΦST comparisons, and multivariate analyses. Eighty-eight haplotypes were identified, showing high haplotype diversity (Hd = 0.767–0.945) and moderate nucleotide diversity (π = 0.0026–0.0054). Most genetic variation occurred within populations, and overall analyses indicated genetic homogeneity. However, pairwise analysis and AMOVA confirmed significant differentiation of the Azores population. These results confirm extensive genetic connectivity throughout the Atlantic–Mediterranean range of P. bogaraveo, likely due to a combination of large larval dispersal and a common spawning migration strategy, but identify the Azores as a genetically distinct unit. This highlights the need to consider both large-scale connectivity and local divergence in fisheries management. Full article