PLoS Genetics最新文献

{"title":"The transcription factors Tfeb and Tfe3 are required for survival and embryonic development of pancreas and liver in zebrafish.","authors":"Alberto Rissone, Martina La Spina, Erica Bresciani, Zulfeqhar A Syed, Christian A Combs, Martha Kirby, Abdel Elkahloun, Vicky Chen, Raman Sood, Shawn M Burgess, Rosa Puertollano","doi":"10.1371/journal.pgen.1011754","DOIUrl":"10.1371/journal.pgen.1011754","url":null,"abstract":"<p><p>The transcription factors TFEB and TFE3 modulate expression of lysosomal, autophagic, and metabolic genes to restore energy and cellular homeostasis in response to a variety of stress conditions. Since their role during vertebrate development is less characterized, we used CRISPR/Cas9 to deplete tfeb, tfe3a, and tfe3b in zebrafish. The simultaneous lack of these genes compromised embryo survival during early development, with an almost complete lethality of the larvae by 8-10 dpf. The knockout animals showed apoptosis in brain and retina and alterations in pancreas, liver, and gut. Exocrine pancreas presented the most severe defects, with accumulation of abnormal zymogen granules leading to acinar atrophy in embryos and pancreatitis-like phenotypes in adults; likely due to a block of the autophagy machinery implicated in removal of damaged granules. Knockout animals displayed increased susceptibility to oxidative and heat-shock stress. Our work reveals an essential role of Tfeb and Tfe3 in maintaining cellular and tissue homeostasis during development.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 6","pages":"e1011754"},"PeriodicalIF":4.0,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12225984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional analysis of CYP4B1 enzymes from apes and humans uncovers evolutionary hot spots for adaptations of the catalytical function.","authors":"Saskia Hüsken, Annika Röder, Johannes Ptok, Anne E Meyer, Mats Georg, Yannick Schwarz, Christian Roos, Kerstin Mätz-Rensing, Michael C Hutter, Doreen M Floss, Allan E Rettie, Marco Girhard, Helmut Hanenberg, Constanze Wiek","doi":"10.1371/journal.pgen.1011750","DOIUrl":"10.1371/journal.pgen.1011750","url":null,"abstract":"<p><p>A hallmark of the highly conserved CYP4B1 enzyme in mammals is the capability to bioactivate both xenobiotic and endobiotic substrates. However, due to a single amino acid change (p.P427S) within the evolutionary conserved meander region no catalytic activity of the native human CYP4B1 has been identified so far. To identify at which point in human evolution the loss of CYP4B1 activity had occurred, we evaluated the activities of CYP4B1 orthologs from 14 primate genera against 4-ipomeanol and perilla ketone in human liver cells. The activity of recombinant CYP4B1 proteins isolated from E. coli was also tested against 4-ipomeanol and lauric acid. Surprisingly, CYP4B1 already became catalytically inactive at the split between apes and monkeys; all tested CYP4B1 orthologs from monkeys were able to bioactivate both protoxins and to hydroxylate lauric acid. Amino acid analysis of the CYP4B1 orthologs revealed four additional evolutionary changes, each affecting the function of ape and human enzymes: p.V71G specific for Denisovans, p.R106C, p.R244H, and an exon deletion found only in the gorilla CYP4B1. Systematic functional analyses proved the negative impact of the genetic changes on CYP4B1 activity and showed that reversion of the mutations restored enzyme activity. The occurrence of five independent inactivating genetic changes in the same gene of closely related species is a clear indication of the importance of inactivating CYP4B1 in apes and humans. Elucidating the evolutionary trigger(s) for CYP4B1 inactivation in our ancestors will ultimately improve our understanding of primate evolution.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 6","pages":"e1011750"},"PeriodicalIF":4.0,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12233900/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Strain background interacts with chromosome 7 aneuploidy to determine commensal and virulence phenotypes in Candida albicans.","authors":"Abhishek Mishra, Norma V Solis, Siobhan M Dietz, Audra L Crouch, Scott G Filler, Matthew Z Anderson","doi":"10.1371/journal.pgen.1011650","DOIUrl":"10.1371/journal.pgen.1011650","url":null,"abstract":"<p><p>The human fungal pathobiont Candida albicans displays extensive genomic plasticity, including large-scale chromosomal changes such as aneuploidy. Chromosome trisomy appears frequently in natural and laboratory strains of C. albicans. Trisomy of specific chromosomes has been linked to large phenotypic effects, such as increased murine gut colonization by strains trisomic for chromosome 7 (Chr7). However, studies of whole-chromosome aneuploidy are generally limited to the SC5314 genome reference strain, making it unclear whether the imparted phenotypes are conserved across C. albicans genetic backgrounds. Here, we report the presence of a Chr7 trisomy in the \"commensal-like\" oral candidiasis strain, 529L, and dissect the contribution of Chr7 trisomy to colonization and virulence in 529L and SC5314. These experiments show that strain background and homolog identity (i.e., AAB vs ABB) interact with Chr7 trisomy to alter commensal and virulence phenotypes in multiple host niches. In vitro filamentation was consistently reduced by Chr7 trisomy in SC5314, but this result was not consistent for 529L. Oral colonization of mice was increased by the presence of a Chr7 trisomy in 529L but not SC5314; conversely, virulence during systemic infection was reduced by Chr7 trisomy in SC5314 but not 529L. Strikingly, the AAB Chr7 trisomy in the SC5314 background rendered this strain avirulent in murine systemic infection. Increased dosage of NRG1 failed to reproduce most of the Chr7 trisomy phenotypes. Our results demonstrate that aneuploidy interacts with background genetic variation to produce complex phenotypic patterns that deviate from our current understanding in the genome reference strain.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 6","pages":"e1011650"},"PeriodicalIF":4.0,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12204564/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural basis for higher-order DNA binding by a bacterial transcriptional regulator.","authors":"Frederik Oskar Graversgaard Henriksen, Lan Bich Van, Ditlev Egeskov Brodersen, RagnhildBager Skjerning","doi":"10.1371/journal.pgen.1011749","DOIUrl":"10.1371/journal.pgen.1011749","url":null,"abstract":"<p><p>Transcriptional regulation by binding of transcription factors to palindromic sequences in promoter regions is a fundamental process in bacteria. Some transcription factors have multiple dimeric DNA-binding domains, in principle enabling interaction with higher-order DNA structures; however, mechanistic and structural insights into this phenomenon remain limited. The Pseudomonas putida toxin-antitoxin (TA) system Xre-RES has an unusual 4:2 stoichiometry including two potential DNA-binding sites, compatible with a complex mechanism of transcriptional autoregulation. Here, we show that the Xre-RES complex interacts specifically with a palindromic DNA repeat in the promoter in a 1:1 molar ratio, leading to transcriptional repression. We determine the 2.7 Å crystal structure of the protein-DNA complex, revealing an unexpected asymmetry in the interaction and suggesting the presence of a secondary binding site, which is supported by structural prediction of the binding to the intact promoter region. Additionally, we show that the antitoxin can be partially dislodged from the Xre-RES complex, resulting in Xre monomers and a 2:2 Xre-RES complex, neither of which repress transcription. These findings highlight a dynamic, concentration-dependent model of transcriptional autoregulation, in which the Xre-RES complex transitions between a non-binding (2:2) and a DNA-binding (4:2) form.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 6","pages":"e1011749"},"PeriodicalIF":4.0,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12204516/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transposable element expression is associated with sex chromosome number in humans.","authors":"Jordan Teoli, Miriam Merenciano, Marie Fablet, Anamaria Necsulea, Daniel Siqueira-de-Oliveira, Alessandro Brandulas-Cammarata, Audrey Labalme, Hervé Lejeune, Jean-François Lemaitre, François Gueyffier, Damien Sanlaville, Claire Bardel, Cristina Vieira, Gabriel Ab Marais, Ingrid Plotton","doi":"10.1371/journal.pgen.1011668","DOIUrl":"10.1371/journal.pgen.1011668","url":null,"abstract":"<p><p>Why women live longer than men is still an open question in human biology. Sex chromosomes have been proposed to play a role in the observed sex gap in longevity, and the Y male chromosome has been suspected of having a potential toxic genomic impact on male longevity. It has been hypothesized that transposable element (TE) repression declines with age, potentially leading to detrimental effects such as somatic mutations and disrupted gene expression, which may accelerate the aging process. Given that the Y chromosome is rich in repeats, age-related increases in TE expression could be more pronounced in males, likely contributing to their reduced longevity compared to females. In this work, we first studied whether TE expression is associated with the number of sex chromosomes in humans. We analyzed blood transcriptomic data obtained from individuals of different karyotype compositions: 46,XX females (normal female karyotype), 46,XY males (normal male karyotype), as well as males with abnormal karyotypes, such as 47,XXY, and 47,XYY. We found that sex chromosomes might be associated to TE expression, with the presence and number of Y chromosomes particularly associated with a global increase in TE expression. This tendency was also observed across several TE subfamilies. We also tested whether TE expression is higher in older males than in older females using published human blood transcriptomic data from the Genotype-Tissue Expression (GTEx) project. However, we did not find increased TE expression in older males compared to older females probably due to the heterogeneity of the dataset. Our findings suggest an association between sex chromosome content and TE expression and open a new window to study the toxic effect of the Y chromosome in human longevity.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 6","pages":"e1011668"},"PeriodicalIF":4.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12225981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144508967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Performance of two low-threshold population replacement gene drives in cage populations of the yellow fever mosquito, Aedes aegypti.","authors":"Zachary J Speth, David G Rehard, Patricia J Norton, Alexander W E Franz","doi":"10.1371/journal.pgen.1011757","DOIUrl":"10.1371/journal.pgen.1011757","url":null,"abstract":"<p><p>Aedes aegypti is the predominant vector for arboviruses including dengue, Zika, and chikungunya viruses, which infect over 100 million people annually. Mosquito population replacement in which arbovirus-susceptible mosquitoes in the field are replaced by laboratory-engineered refractory mosquitoes represents a novel genetic control measure to interrupt arboviral disease cycles. For this approach, the engineered mosquitoes need to harbor two genetic components: an antiviral effector construct which is linked to a gene drive (GD). We tested the performance of two single-locus CRISPR/Cas9 based GD for Ae. aegypti population replacement in small cage populations for up to 16 generations. Starting from a low release threshold of 1:9 GD bearing males to wild-type males, we observed two GD constructs in which Cas9 was expressed from two different germline promoters, nanos and zpg, to increase in frequency in all cage populations. By G16, an average of 72% and 82% of individuals from the zpg-GD and nanos-GD populations, respectively, harbored at least one GD copy with corresponding increases in allele frequencies. This indicated that the two single-locus, CRISPR/Cas9-based homing GD exhibited continuous super-Mendelian inheritance in populations of Ae. aegypti. Gene drive blocking indel (GDBI, a.k.a. \"resistant alleles\") frequency was measured for each discrete generation in pooled samples from the six populations harboring GD. We found that populations with Cas9 expression under control of the nanos-promoter accumulated GDBI at more than twice the rate of those populations harboring the zpg-promoter driven GD. Based on preexisting data sets for homing and GDBI frequencies in addition to the cage trial observations, the relative contributions of sex-specific homing rates, maternal Cas9 deposition and potential fitness effects were modeled in MGDrivE for both GD, further explaining their divergent performance. Our study demonstrates the feasibility of low-threshold, single-locus CRISPR/Cas9 based GD for Ae. aegypti population replacement.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 6","pages":"e1011757"},"PeriodicalIF":4.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12221180/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144508966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Defining the high-translational readthrough stop codon context.","authors":"Daniela Smoljanow, Dennis Lebeda, Julia Hofhuis, Sven Thoms","doi":"10.1371/journal.pgen.1011753","DOIUrl":"10.1371/journal.pgen.1011753","url":null,"abstract":"<p><p>Translational termination is not entirely efficient and competes with elongation, which might result in translational readthrough (TR). TR occurs when a near-cognate tRNA binds to a stop codon, (mis)interpreting it as a sense codon and producing a C-terminal extension of the protein. This process is influenced by the stop codon itself and the surrounding nucleotide sequence, known as the stop codon context (SCC). To investigate the role of these cis-acting elements beyond the high-TR motif UGA CUA G, this study examines specific positions within the SCC, both upstream and downstream of the motif, that contribute to variations in basal and aminoglycoside-induced TR. In particular, we identified a surprisingly large influence of the upstream nucleotide positions -9 and -8 (relative to the stop codon) and positions +11 and +12 on readthrough levels, revealing a complex interplay between nucleotides in the expanded SCC with effects turning out to be non-linear and, furthermore, not transferable to evolutionarily non-adapted SCCs. These findings support our understanding of translational termination and may benefit the development of pharmacological therapy for diseases caused by premature stop codon mutations.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 6","pages":"e1011753"},"PeriodicalIF":4.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12233894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144498815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic disease risks of under-represented founder populations in New York City.","authors":"Mariko Isshiki, Anthony J Griffen, Paul Meissner, Paulette Spencer, Michael D Cabana, Susan D Klugman, Mirtha Colón, Zoya Maksumova, Shakira Suglia, Carmen R Isasi, John M Greally, Srilakshmi M Raj","doi":"10.1371/journal.pgen.1011755","DOIUrl":"10.1371/journal.pgen.1011755","url":null,"abstract":"<p><p>The detection of founder pathogenic variants, those observed in high frequency only in a group of individuals with increased inter-relatedness, can help improve delivery of health care for that community. We identified 16 groups with shared ancestry, based on genomic segments that are shared through identity by descent (IBD), in New York City using the genomic data of 25,366 residents from the All Of Us Research Program and the Mount Sinai BioMe biobank. From these groups we defined 7 as founder populations, mostly communities currently under-represented in medical genomics research, such as Puerto Rican and Garifuna. The enrichment analysis of ClinVar pathogenic or likely pathogenic (P/LP) variants in each group identified 201 of these damaging variants across the seven founder populations. We confirmed disease-causing variants previously reported to occur at increased frequencies in Ashkenazi Jewish and Puerto Rican genetic ancestry groups, but most of the damaging variants identified have not been previously associated with any such founder populations, and most of these founder populations have not been described to have increased prevalence of the associated rare disease. Twenty-two of 47 variants meeting Tier 2 prenatal screening criteria (1/100 carrier frequency within these founder groups) have never previously been reported. We show how population structure studies can provide insights into rare diseases disproportionately affecting under-represented founder populations, delivering a health care benefit but also a potential source of stigmatization of these communities, who should be part of the decision-making about implementation into health care delivery.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 6","pages":"e1011755"},"PeriodicalIF":4.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12208467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144486760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inheritance bias of deletion-harbouring mtDNA in yeast: The role of copy number and intracellular selection.","authors":"Nataliia D Kashko, Georgii Muravyov, Iuliia Karavaeva, Elena S Glagoleva, Maria D Logacheva, Sofya K Garushyants, Dmitry A Knorre","doi":"10.1371/journal.pgen.1011737","DOIUrl":"10.1371/journal.pgen.1011737","url":null,"abstract":"<p><p>During sexual reproduction, fungi usually inherit mtDNA from both parents, however, the distribution of the mtDNA in the progeny can be biased toward some mtDNA variants. For example, crossing Saccharomyces cerevisiae strain carrying wild type (rho+) mtDNA with the strain carrying mutant mtDNA variant with a large deletion (rho-) can produce up to 99-100% of rho- diploid progeny. Two factors could contribute to this phenomenon. First, rho- cells may accumulate more copies of mtDNA molecules per cell than wild-type cells, making rho- mtDNA the prevalent mtDNA molecule in zygotes. This consequently leads to a high portion of rho- diploid cells in the offspring. Second, rho- mtDNA may have a competitive advantage within heteroplasmic cells, and therefore could displace rho+ mtDNA in a series of generations, regardless of their initial ratio. To assess the contribution of these factors, we investigated the genotypes and phenotypes of twenty two rho- yeast strains. We found that indeed rho- cells have a higher mtDNA copy number per cell than rho+ strains. Using an in silico modelling of mtDNA selection and random drift in heteroplasmic yeast cells, we assessed the intracellular fitness of mutant mtDNA variants. Our model indicates that both higher copy numbers and intracellular fitness advantage of the rho- mtDNA contribute to the biased inheritance of rho- mtDNA.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 6","pages":"e1011737"},"PeriodicalIF":4.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12186888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144486761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct domains of ENHANCER OF PINOID hold information for its polarization required for auxin-mediated cotyledon and flower development in Arabidopsis.","authors":"Michaela S Matthes, Nicole Yun, Miriam Luichtl, Ulrich Büschges, Birgit S Fiesselmann, Benjamin Strickland, Marietta S Lehnardt, Kay Schneitz, Klaus Michel, Ramon A Torres Ruiz","doi":"10.1371/journal.pgen.1011217","DOIUrl":"10.1371/journal.pgen.1011217","url":null,"abstract":"<p><p>The Arabidopsis ENHANCER OF PINOID (ENP) protein and the AGC-kinase PINOID (PID) synergistically impact on polarization and function of the auxin transporter PIN-FORMED1 (PIN1) required for plant leaf and flower organ development. ENP offers a PID-independent input for PIN-function since enp pid double mutants lead to cotyledon- and flower-less plants in contrast to pid single mutants, which develop cotyledons and abnormal albeit fertile flowers. This indicates that ENP, which depicts a similar polar localization as PIN1, is a potential interactor of PINs including PIN1. Here we show that the modular structure of ENP predicted by AlphaFold separates the capability for its own cellular polarization and its function linked to polar PIN1 activity. The part of ENP from aa1 to aa470 is subdivided into three structured domains. They are supportive and/or essential for cellular polarity. In contrast, the C-terminus, which is an intrinsically disordered region (IDR), is completely dispensable for polarity but essential for ENP-mediated PIN1-function. FLIM-FRET shows ENP to be closely associated with the plasma membrane and its IDR to significantly interact with PINs. Moreover, the modification status of two prominent phosphorylation sites in the IDR determines ENPs stability and its capability in supporting PIN1. Our results show ENP to be an element in the assumed PIN-multiprotein complex and explain its impact on PID-independent PIN1 activity.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 6","pages":"e1011217"},"PeriodicalIF":4.0,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12201645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144477549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}