Molecular Genetics and Genomics最新文献

{"title":"The causality between physical activity and gestational diabetes mellitus: a Mendelian randomization study.","authors":"Xiaoyan Ma, Yanqiu Liu, Xia Xu, Hua Wang, Xiaosu Zhao","doi":"10.1007/s00438-026-02430-2","DOIUrl":"10.1007/s00438-026-02430-2","url":null,"abstract":"<p><p>Although observational research shows that physical activity and sedentary behavior are associated with the risk of gestational diabetes mellitus (GDM), lipid, and body mass index (BMI), their causal direction and potential mediating mechanism are still unclear, which limits the development of precise prevention strategies. Based on the genetic data on the European ancestry population, the study aimed to investigate the causal relationship of GDM with physical activity and sedentary behavior using Mendelian randomization (MR), and quantify the mediating roles of BMI and lipids in it. The bidirectional dual sample MR analysis based on whole genome association research data revealed that there was a significant negative causal association between physical activity time and the risk of GDM in females (OR = 0.977, 95% CI: 0.956-0.998, P = 0.030), while leisure screen time had a positive causal association with the risk of developing GDM (OR = 1.125, 95% CI: 1.023-1.238, P = 0.015). Mediation analysis indicated that BMI was the primary causal pathway for reducing the risk of GDM through physical activity time, with a mediation ratio of 53.6%. Multivariate MR analysis showed that after adjusting for BMI, the direct effect was no longer significant, indicating that BMI played a major and almost complete mediating role. In the causal pathway of increased GDM risk in leisure screen time, BMI, high-density lipoprotein cholesterol (HDL-C), and Apolipoprotein A1 (ApoA1) effectively mediated the causal relationship between leisure screen time and GDM risk, with mediation proportions of 81.8%, 11.2% and 10.1%, respectively. Physical activity can indirectly reduce the risk of GDM by lowering BMI, while excessive leisure screen time significantly increases the risk of GDM by affecting BMI, HDL-C, and ApoA1. These findings support the potential value of prioritizing weight control and integrating interventions that increase physical activity and limit sedentary behavior as core measures, in order to fundamentally block the pathway of GDM by synergistically optimizing weight and lipid metabolism.</p>","PeriodicalId":18816,"journal":{"name":"Molecular Genetics and Genomics","volume":"301 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148033172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FAM72A is associated with lung cancer proliferation and migration via the NF‑κB signaling pathway.","authors":"Qinhua Gu, Qibin Shen, Tiancheng Liu, Lili Jin, Weiwei Min","doi":"10.1007/s00438-026-02450-y","DOIUrl":"10.1007/s00438-026-02450-y","url":null,"abstract":"<p><p>Lung cancer remains the leading cause of cancer-related deaths worldwide. While the Family with sequence similarity 72 member A (FAM72A) gene has been implicated in various cancers, its role in lung cancer is yet to be determined. This study aimed to investigate the role of FAM72A in lung cancer and the underlying mechanism. Bioinformatic analysis of The Cancer Genome Atlas-Lung Adenocarcinoma (TCGA-LUAD) dataset revealed that FAM72A was significantly upregulated in lung adenocarcinoma tissues, and high FAM72A expression was closely associated with poor patient prognosis. Western blot analysis revealed that FAM72A protein expression was significantly upregulated in multiple lung cancer cell lines (A549, H1299, and H460) compared to normal lung epithelial cells. Through a series of assays including flow cytometry, MTT, clone formation, wound healing, and Transwell experiments, we demonstrated that knockdown of FAM72A via shRNA effectively suppressed proliferation and migration in A549 and H1299 cells, while promoting apoptosis. Additionally, in vivo studies using a mouse xenograft model confirmed that FAM72A knockdown inhibited tumor growth. Mechanistic analyses showed that FAM72A knockdown is associated with inactivation of the NF‑κB signaling pathway, as knockdown led to decreased expression of p-IkBα, p-IKKα, p-NF-κB, Cyclin D1, and PCNA. In conclusion, our findings demonstrate that FAM72A contributes to lung cancer progression by regulating the activity of the NF‑κB signaling pathway, suggesting its potential as a therapeutic target for lung cancer.</p>","PeriodicalId":18816,"journal":{"name":"Molecular Genetics and Genomics","volume":"301 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148006002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ecotype-specific sensitivity to DNA methylation inhibitors in Arabidopsis cmt3 mutants.","authors":"Xin Sun, Guo Du, Atsushi Kato, Hidetaka Ito","doi":"10.1007/s00438-026-02449-5","DOIUrl":"10.1007/s00438-026-02449-5","url":null,"abstract":"<p><p>DNA methylation inhibitors such as 5-aza-2'-deoxycytidine (5-Aza-2dC) are widely used to probe epigenetic regulation, yet genetic factors underlying natural variation in inhibitor sensitivity remain poorly understood. Here, we investigated ecotype-specific responses to 5-Aza-2dC in Arabidopsis thaliana, focusing on cmt3 mutants in the Columbia (Col-0) and Landsberg erecta (Ler) backgrounds. We found that cmt3 mutants displayed contrasting phenotypes depending on genetic background: Col-0 cmt3 mutants showed relative resistance to 5-Aza-2dC, whereas Ler cmt3 mutants exhibited pronounced sensitivity. Genetic analyses indicated that this enhanced sensitivity in the Ler background is recessive and cannot be explained solely by loss of CMT3 function. Through genetic mapping, we identified At1g34770 (NSE3) as a strong candidate modifier associated with 5-Aza-2dC sensitivity. A non-synonymous substitution in NSE3 correlated with growth inhibition under inhibitor treatment, and transgenic analyses further supported a contributory role for this gene. Together, our results demonstrate that natural genetic modifiers, including allelic variation in NSE3, shape ecotype-dependent responses to DNA methylation inhibition, highlighting the importance of genetic background in modulating epigenetic perturbations in plants.</p>","PeriodicalId":18816,"journal":{"name":"Molecular Genetics and Genomics","volume":"301 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome comparison of the bacteria in Mycobacterium avium complex (MAC) reveals the role of translational selection in shaping codon usage patterns.","authors":"Anindita Banerjee, Saubashya Sur","doi":"10.1007/s00438-026-02447-7","DOIUrl":"10.1007/s00438-026-02447-7","url":null,"abstract":"<p><p>The Mycobacterium avium complex (MAC) houses several pathogens that cause diseases in humans, ruminants, and birds. They are widely distributed in soils and water worldwide. In immunocompromised humans, MAC is responsible for nodular bronchiectasis and fibrocavitary lung diseases. The treatment of lung diseases induced by MAC remains difficult owing to antibiotic intolerance and disease recurrence. In this study, we compared the genome sequences of 90 complete MAC genomes and explored the factors shaping codon usage bias in the bacteria within MAC. Additionally, we studied the relationship between codon bias and pathogenic adaptation. The genome sizes ranged from 4.7 to 6.5 Mb. Variation in the mobile genetic elements and the number of CRISPR candidates was observed amongst the bacteria within MAC. Synonymous codon usage analysis divulged variations among subspecies, high codon usage bias, substantial heterogeneity in codon usage patterns, and moderate use of optimal codons. High GC3 content and elevated levels of CAI (a metric for gene expression levels) in all probability assisted the bacteria within MAC in adjusting to different host environments. Translational selection pressure prevailed over compositional bias and mutational selection in these organisms. Our analysis revealed differences in the tRNA content amongst the bacteria in MAC. The translational selective pressure enabled the adaptation of these pathogenic bacteria to competitive pressure in diverse environments and niches by maintaining a lesser number of tRNAs and lower tAI values.</p>","PeriodicalId":18816,"journal":{"name":"Molecular Genetics and Genomics","volume":"301 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147973326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated transcriptomic and metabolomic investigation reveals that graphene oxide reduces nicosulfuron detriment in sweet corn.","authors":"Yanli Wang, Xuemei Zhong, Meng Zhang, Jian Wang","doi":"10.1007/s00438-026-02452-w","DOIUrl":"10.1007/s00438-026-02452-w","url":null,"abstract":"<p><p>Nicosulfuron (NIF) stress poses a significant constraint on sweet corn production. Graphene oxide (GO), as an environmentally friendly nanomaterial, serves as a safe agent to enhance crop stress resistance. However, the molecular mechanisms of GO-mediated sweet corn to tolerate NIF remain largely unexplored. This study aimed to investigate the regulatory effects of GO on sweet corn's response to NIF through physiological assessments, comparative transcriptomic analysis, and metabolomic profiling. The findings indicate that the application of GO mitigates the detrimental effects of NIF stress on sweet corn seedlings, as evidenced by enhanced growth metrics, improved chlorophyll fluorescence parameters, and photosynthetic indicators. GO predominantly influences genes and metabolites related to the synthesis of flavonoids, phenylpropanoids, and calcium (Ca²⁺) signaling pathways to counteract NIF stress in sweet corn. Additionally, key genes associated with peroxidases (POD) and cytochrome P450 monooxygenases (CYP) were identified through the analysis of weighted gene co-expression networks (WGCNA). These genes play crucial roles in the response to NIF stress orchestrated by graphene oxide. In summary, this study demonstrates the synergistic regulatory effect of GO on NIF tolerance in sweet corn, providing valuable insights for developing NIF-resistant sweet corn varieties.</p>","PeriodicalId":18816,"journal":{"name":"Molecular Genetics and Genomics","volume":"301 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147973906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ProSSF: integrating sequence, structure, and gene ontology for prediction of protein stability, interaction, and function.","authors":"Tongqiang Jiang, Yongshan Zhu, Zhenqiao Liu, Xiaowei Yi, Qingchuan Zhang, Shaoyi Song","doi":"10.1007/s00438-026-02433-z","DOIUrl":"10.1007/s00438-026-02433-z","url":null,"abstract":"<p><p>Protein sequences encode rich structural and functional information that governs how organisms respond to genetic variation, environmental challenge, and disease. However, existing computational methods typically rely on a single information source, whether sequence, structure, or functional annotation, and their predictive power is substantially reduced for low-homology proteins or orphan proteins. Here we present ProSSF (Protein Sequence-Structure-Function), a unified multimodal pretraining framework that performs masked pretraining on large-scale protein sequences, encodes three-dimensional structural information via a Geometric Vector Perceptron Graph Neural Network (GVP-GNN), integrates Gene Ontology (GO) semantics through a dual-path hierarchical encoder, and aligns all three modalities into a shared representation space via cross-modal attention. Evaluated across three downstream tasks, ProSSF achieves a Spearman correlation of 0.74 ± 0.009 on the TAPE protein stability benchmark, a mean Micro-F1 of 84.60% ± 0.9% on the SHS148K protein-protein interaction dataset under the stringent DFS partition, and comparable or superior Fmax and AUPR relative to state-of-the-art baselines across all three GO sub-ontologies. Ablation analyses demonstrate that structural geometry and GO functional semantics contribute complementary and task-dependent information, with the largest performance gains observed under low-homology conditions. Attention-based interpretability analyses further reveal that the model preferentially attends to biologically meaningful regions, such as kinase catalytic domains, without explicit supervision. This study provides a unified multimodal pretraining framework and demonstrates that jointly encoding sequence, structure, and functional semantics substantially improves the generalizability of protein property prediction. Future studies should validate this framework on larger, taxonomically diverse protein datasets and explore its potential applications in the functional annotation of disease-associated proteins and the identification of novel drug targets.</p>","PeriodicalId":18816,"journal":{"name":"Molecular Genetics and Genomics","volume":"301 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147973961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microenvironmental pH and host-pathogen co-evolution potentially influence the structural architecture of junctional adhesion molecules.","authors":"Taner Karagöl, Alper Karagöl","doi":"10.1007/s00438-026-02444-w","DOIUrl":"10.1007/s00438-026-02444-w","url":null,"abstract":"<p><p>Understanding how proteins dynamically adapt to diverse and changing physiological microenvironments is a fundamental challenge in modern biological sciences. Junctional adhesion molecules (JAMs) are a family of conserved proteins critically involved in immune regulation and cell adhesion. In this study, we investigate the evolutionary and structural dynamics of three paralogs across 274 mammalian taxa, which share similar tertiary structures but differ in isoelectric points (pI). By integrating phylogenetic modeling, partial correlation, network topology, and evolutionary molecular dynamics in physiological pH (6.5-10.5) gradient, we explored potential explanations driving this diversification. Our analysis identified JAM-B as a likely central node in the conservation network, with Lys and Cys residues as central evolutionary residues. Evolutionary mapping revealed recent episodic selection bursts across 17% to 26% of mammalian lineages, could indicate that specific functional interfaces are undergoing rapid, lineage-specific innovation. Notably, we identified episodic hotspots in JAM-A at the distal D1 viral entry interface, consistent with an ongoing host-pathogen arms race, and parallel adaptive clusters at the C-terminal motifs across all paralogs. AlphaMissense profiling revealed that acidic-> basic mutations exhibit significantly lower pathogenicity scores. In preliminary early-onset dynamics simulations, root-mean-square-deviation profiles could suggest a pI-stability relationship, JAM-A and JAM-C displayed biphasic pH-dependent deviations (at pH 8.0 and pH 8.5). Dynamics-aware evolutionary profiling identified key dynamic-conserved residues: JAM-A at Gln66, JAM-B at Gln36 and Val57, and JAM-C at several basic residues. Together, these results suggest that isoelectric divergence correlates with residue evolution and microenvironment-specific structural dynamics. Ultimately, our integrated computational framework provides genomic insights into paralog diversification, offering a testable architectural blueprint for targeted mutagenesis or therapeutic modulation of pH-sensitive adhesion processes.</p>","PeriodicalId":18816,"journal":{"name":"Molecular Genetics and Genomics","volume":"301 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147973969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional characterization and allele-specific RNA interference-based rescue of KCNH2 p.F68C variant associated with long QT syndrome.","authors":"Miao Zhao, Meng Han, Wenjuan Li, Zhijie Wang, Li Chen, Hanyu Zeng, Ziqi Zhou, Dongping Hu, Yu Cheng, Qing Wang, Tie Ke","doi":"10.1007/s00438-026-02442-y","DOIUrl":"10.1007/s00438-026-02442-y","url":null,"abstract":"<p><p>Long QT syndrome (LQTS) is an inherited life-threatening cardiac disorder characterized by delayed ventricular repolarization and increased risk of malignant arrhythmias. Among its subtypes, long QT syndrome type 2 (LQT2) is primarily caused by pathogenic variants in KCNH2, which encodes the human ether-à-go-go-related gene (hERG) potassium channel responsible for the rapid delayed rectifier current (I_Kr). However, the substantial functional heterogeneity among KCNH2 variants poses a major challenge for clinical interpretation and precision intervention. In this study, we sought to functionally characterize KCNH2 p.F68C variant (c.203T > G) identified in a Chinese LQT2 patient and to evaluate the feasibility of RNA interference-based modulation of its functional impact on the hERG channel. Using biochemical and electrophysiological analyses in HEK293T cells, we show that variant p.F68C causes a severe trafficking defect and exerts a dominant-negative effect on wild-type hERG channels, leading to markedly reduced rapid delayed rectifier potassium current (I_Kr). In contrast to several previously reported Per-Arnt-Sim (PAS) domain variants, the trafficking defect of p.F68C was resistant to reduced culture temperature, chemical chaperones, and pharmacological chaperones. Notably, allele-specific RNA interference selectively suppressed mutant hERG expression, alleviated dominant-negative interference, and partially restored hERG current density without detectable cytotoxicity. Together, these findings establish p.F68C as a loss-of-function KCNH2 variant and highlight allele-specific RNA interference as a variant-directed strategy that may serve as an alternative to suppression-replacement approaches, providing a basis for functional interpretation and precision therapeutic exploration of individual KCNH2 variants.</p>","PeriodicalId":18816,"journal":{"name":"Molecular Genetics and Genomics","volume":"301 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KIRREL1 is a novel prognostic biomarker that promotes malignancy in gastric cancer via activation of the epithelial-mesenchymal transition pathway.","authors":"Huohua Lv, Jun Liu, Lufei Jiang, ZhiWen Nie, Yaoxin Wang","doi":"10.1007/s00438-026-02438-8","DOIUrl":"10.1007/s00438-026-02438-8","url":null,"abstract":"<p><p>Gastric cancer (GC) is a leading cause of cancer-related mortality characterized by aggressive metastasis and limited therapeutic options. Kin of IRRE-like protein 1 (KIRREL1) is an emerging cell surface protein whose specific oncogenic role in GC remains largely unknown. Therefore, the intention of this study was to comprehensively investigate the clinical relevance, biological functions, and underlying molecular mechanisms of KIRREL1 in GC progression. The expression and prognostic value of KIRREL1 were evaluated using data from The Cancer Genome Atlas (TCGA) and in vitro experiments. Gain- and loss-of-function studies were performed in GC cell lines to assess the effects of KIRREL1 on proliferation, 5-FU chemosensitivity, migration, and invasion. Western blotting was used to examine the regulation of epithelial-mesenchymal transition (EMT) markers. KIRREL1 was significantly upregulated in GC tissues and cell lines, and its high expression was strongly correlated with poor progression-free, disease-specific, and overall survival in patients. Functionally, KIRREL1 overexpression promoted GC cell proliferation, migration, and invasion, whereas its knockdown had the opposite effects. Furthermore, KIRREL1 knockdown sensitized GC cells to 5-FU treatment. Mechanistically, KIRREL1 was found to positively regulate the expression of the key EMT markers Vimentin, MMP2, and MMP9. Our findings identify KIRREL1 as a novel oncogene that actively promotes GC proliferation, 5-FU chemoresistance, and metastasis via the EMT pathway. Importantly, this establishes KIRREL1 as both a robust prognostic biomarker and a targetable driver of malignancy. Future clinical perspectives should explore the development of specific KIRREL1 inhibitors to overcome chemoresistance and suppress metastatic dissemination.</p>","PeriodicalId":18816,"journal":{"name":"Molecular Genetics and Genomics","volume":"301 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147973956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial genomes from RNA-Seq reveal phylogeny and selection in Mepraia (Hemiptera: Reduviidae).","authors":"Matheus Cardoso de Siqueira E Silva, José Paulo Leite Guadanucci, Tiago Belintani","doi":"10.1007/s00438-026-02434-y","DOIUrl":"10.1007/s00438-026-02434-y","url":null,"abstract":"<p><p>Despite the epidemiological importance of triatomine bugs as vectors of Trypanosoma cruzi, mitogenomic resources remain limited for many lineages, restricting evolutionary and comparative analyses. The endemic Chilean genus Mepraia is a notable example, with scarce mitochondrial genomic information despite its relevance to Chagas disease ecology and vector evolution. Here, we reconstructed partial mitochondrial genomes, including all 13 protein-coding genes, from RNA-Seq data for three Mepraia species. Phylogenetic analyses confirmed the monophyly of Mepraia and resolved interspecific relationships, whereas comparative analyses revealed heterogeneous patterns of intraspecific diversity, with elevated variation in M. parapatrica. Codon-based tests detected pervasive purifying selection together with localized signals of positive selection in oxidative phosphorylation genes, particularly NAD5, NAD6, NAD1, and COIII. These results show that transcriptomic data provide a reliable source for mitochondrial genome reconstruction in non-model insects and that adaptive signals can coexist with strong functional constraint in triatomine mitogenomes. Overall, this study expands mitogenomic resources for Triatominae, improves evolutionary inference in Mepraia, and provides a foundation for future integrative studies on diversification, mitochondrial evolution, and vector biology.</p>","PeriodicalId":18816,"journal":{"name":"Molecular Genetics and Genomics","volume":"301 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147973925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}