PLoS Genetics最新文献

{"title":"Refining fine-mapping: Effect sizes and regional heritability.","authors":"Christian Benner, Mahajan Anubha, Matti Pirinen","doi":"10.1371/journal.pgen.1011480","DOIUrl":"https://doi.org/10.1371/journal.pgen.1011480","url":null,"abstract":"<p><p>Recent statistical approaches have shown that the set of all available genetic variants explains considerably more phenotypic variance of complex traits and diseases than the individual variants that are robustly associated with these phenotypes. However, rapidly increasing sample sizes constantly improve detection and prioritization of individual variants driving the associations between genomic regions and phenotypes. Therefore, it is useful to routinely estimate how much phenotypic variance the detected variants explain for each region by taking into account the correlation structure of variants and the uncertainty in their causal status. Here we extend the FINEMAP software to estimate the effect sizes and regional heritability under the probabilistic model that assumes a handful of causal variants per region. Using the UK Biobank (UKB) data to simulate genomic regions, we demonstrate that FINEMAP provides higher precision and enables more detailed decomposition of regional heritability into individual variants than the variance component model implemented in BOLT or the fixed-effect model implemented in HESS, particularly when there are only a few causal variants in the fine-mapped region. Using data from 2,940 plasma proteins from the UKB study, we observed that on average FINEMAP identified 2.5 causal variants at an association signal and captured 36% more regional heritability than the variant with the lowest P-value. We estimate that in genomic regions with notable contribution to the total heritability, FINEMAP captures on average 13% and 40% more heritability than BOLT and HESS respectively. Our analysis shows how FINEMAP, BOLT and HESS relate to each other in cases where inference of a variant-level picture of the regional genetic architecture is possible.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 1","pages":"e1011480"},"PeriodicalIF":4.0,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142957263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Estimating evolutionary and demographic parameters via ARG-derived IBD.","authors":"Zhendong Huang, Jerome Kelleher, Yao-Ban Chan, David Balding","doi":"10.1371/journal.pgen.1011537","DOIUrl":"10.1371/journal.pgen.1011537","url":null,"abstract":"<p><p>Inference of evolutionary and demographic parameters from a sample of genome sequences often proceeds by first inferring identical-by-descent (IBD) genome segments. By exploiting efficient data encoding based on the ancestral recombination graph (ARG), we obtain three major advantages over current approaches: (i) no need to impose a length threshold on IBD segments, (ii) IBD can be defined without the hard-to-verify requirement of no recombination, and (iii) computation time can be reduced with little loss of statistical efficiency using only the IBD segments from a set of sequence pairs that scales linearly with sample size. We first demonstrate powerful inferences when true IBD information is available from simulated data. For IBD inferred from real data, we propose an approximate Bayesian computation inference algorithm and use it to show that even poorly-inferred short IBD segments can improve estimation. Our mutation-rate estimator achieves precision similar to a previously-published method despite a 4 000-fold reduction in data used for inference, and we identify significant differences between human populations. Computational cost limits model complexity in our approach, but we are able to incorporate unknown nuisance parameters and model misspecification, still finding improved parameter inference.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 1","pages":"e1011537"},"PeriodicalIF":4.0,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142957347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Light-regulated microRNAs shape dynamic gene expression in the zebrafish circadian clock.","authors":"Zuo Wang, Shuang Wang, Yi Bi, Alessandra Boiti, Shengxiang Zhang, Daniela Vallone, Xianyong Lan, Nicholas S Foulkes, Haiyu Zhao","doi":"10.1371/journal.pgen.1011545","DOIUrl":"https://doi.org/10.1371/journal.pgen.1011545","url":null,"abstract":"<p><p>A key property of the circadian clock is that it is reset by light to remain synchronized with the day-night cycle. An attractive model to explore light input to the circadian clock in vertebrates is the zebrafish. Circadian clocks in zebrafish peripheral tissues and even zebrafish-derived cell lines are entrainable by direct light exposure thus providing unique insight into the function and evolution of light regulatory pathways. Our previous work has revealed that light-induced gene transcription is a key step in the entrainment of the circadian clock as well as enabling the more general adaptation of zebrafish cells to sunlight exposure. However, considerable evidence points to post-transcriptional regulatory mechanisms, notably microRNAs (miRNAs), playing an essential role in shaping dynamic changes in mRNA levels. Therefore, does light directly impact the function of miRNAs? Are there light-regulated miRNAs and if so, which classes of mRNA do they target? To address these questions, we performed a complete sequencing analysis of light-induced changes in the zebrafish transcriptome, encompassing small non-coding RNAs as well as mRNAs. Importantly, we identified sets of light-regulated miRNAs, with many regulatory targets representing light-inducible mRNAs including circadian clock genes and genes involved in redox homeostasis. We subsequently focused on the light-responsive miR-204-3-3p and miR-430a-3p which are predicted to regulate the expression of cryptochrome genes (cry1a and cry1b). Luciferase reporter assays validated the target binding of miR-204-3-3p and miR-430a-3p to the 3'UTRs of cry1a and cry1b, respectively. Furthermore, treatment with mimics and inhibitors of these two miRNAs significantly affected the dynamic expression of their target genes but also other core clock components (clock1a, bmal1b, per1b, per2, per3), as well as the rhythmic locomotor activity of zebrafish larvae. Thus, our identification of light-responsive miRNAs reveals new intricacy in the multi-level regulation of the circadian clockwork by light.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 1","pages":"e1011545"},"PeriodicalIF":4.0,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142957352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improving polygenic prediction from summary data by learning patterns of effect sharing across multiple phenotypes.","authors":"Deborah Kunkel, Peter Sørensen, Vijay Shankar, Fabio Morgante","doi":"10.1371/journal.pgen.1011519","DOIUrl":"10.1371/journal.pgen.1011519","url":null,"abstract":"<p><p>Polygenic prediction of complex trait phenotypes has become important in human genetics, especially in the context of precision medicine. Recently, mr.mash, a flexible and computationally efficient method that models multiple phenotypes jointly and leverages sharing of effects across such phenotypes to improve prediction accuracy, was introduced. However, a drawback of mr.mash is that it requires individual-level data, which are often not publicly available. In this work, we introduce mr.mash-rss, an extension of the mr.mash model that requires only summary statistics from Genome-Wide Association Studies (GWAS) and linkage disequilibrium (LD) estimates from a reference panel. By using summary data, we achieve the twin goal of increasing the applicability of the mr.mash model to data sets that are not publicly available and making it scalable to biobank-size data. Through simulations, we show that mr.mash-rss is competitive with, and often outperforms, current state-of-the-art methods for single- and multi-phenotype polygenic prediction in a variety of scenarios that differ in the pattern of effect sharing across phenotypes, the number of phenotypes, the number of causal variants, and the genomic heritability. We also present a real data analysis of 16 blood cell phenotypes in the UK Biobank, showing that mr.mash-rss achieves higher prediction accuracy than competing methods for the majority of traits, especially when the data set has smaller sample size.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 1","pages":"e1011519"},"PeriodicalIF":4.0,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142957350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-modal comparison of molecular programs driving nurse cell death and clearance in Drosophila melanogaster oogenesis.","authors":"Shruthi Bandyadka, Diane P V Lebo, Albert A Mondragon, Sandy B Serizier, Julian Kwan, Jeanne S Peterson, Alexandra Y Chasse, Victoria Jenkins, Anoush Calikyan, Anthony J Ortega, Joshua D Campbell, Andrew Emili, Kimberly McCall","doi":"10.1371/journal.pgen.1011220","DOIUrl":"https://doi.org/10.1371/journal.pgen.1011220","url":null,"abstract":"<p><p>The death and clearance of nurse cells is a consequential milestone in Drosophila melanogaster oogenesis. In preparation for oviposition, the germline-derived nurse cells bequeath to the developing oocyte all their cytoplasmic contents and undergo programmed cell death. The death of the nurse cells is controlled non-autonomously and is precipitated by epithelial follicle cells of somatic origin acquiring a squamous morphology and acidifying the nurse cells externally. Alternatively, stressors such as starvation can induce the death of nurse cells earlier in mid-oogenesis, manifesting apoptosis signatures, followed by their engulfment by epithelial follicle cells. To identify and contrast the molecular pathways underlying these morphologically and genetically distinct cell death paradigms, both mediated by follicle cells, we compared their genome-wide transcriptional, translational, and secretion profiles before and after differentiating to acquire a phagocytic capability, as well as during well-fed and nutrient-deprived conditions. By coupling the GAL4-UAS system to Translating Ribosome Affinity Purification (TRAP-seq) and proximity labeling (HRP-KDEL) followed by Liquid Chromatography tandem mass-spectrometry, we performed high-throughput screens to identify pathways selectively activated or repressed by follicle cells to employ nurse cell-clearance routines. We also integrated two publicly available single-cell RNAseq atlases of the Drosophila ovary to define the transcriptomic profiles of follicle cells. In this report, we describe the genes and major pathways identified in the screens and the striking consequences to Drosophila melanogaster oogenesis caused by RNAi perturbation of prioritized candidates. To our knowledge, our study is the first of its kind to comprehensively characterize two distinct apoptotic and non-apoptotic cell death paradigms in the same multi-cellular system. Beyond molecular differences in cell death, our investigation may also provide insights into how key systemic trade-offs are made between survival and reproduction when faced with physiological stress.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 1","pages":"e1011220"},"PeriodicalIF":4.0,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142928531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polymyositis in Kooiker dogs is associated with a 39 kb deletion upstream of the canine IL21/IL2 locus.","authors":"Yvet Opmeer, Frank G van Steenbeek, Claudia Rozendom, Hille Fieten, Montse M Diaz Espineira, Qurine E M Stassen, Peter J van Kooten, Victor P M G Rutten, Marjo K Hytönen, Hannes Lohi, Paul J J Mandigers, Peter A Leegwater","doi":"10.1371/journal.pgen.1011538","DOIUrl":"10.1371/journal.pgen.1011538","url":null,"abstract":"<p><p>Recently we characterized polymyositis in the Dutch Kooiker dog. The familial occurrence of the disease were suggestive of an inherited cause. Here we report the results of our molecular genetic investigation. A genome-wide association study of 33 cases and 106 controls indicated the involvement of a region on chromosome CFA19 (p = 4.7*10-10). Haplotype analysis indicated that the cases shared a 2.9 Mb region in the homozygous or the heterozygous state. Next Generation Sequencing of genomic DNA implicated a deletion of a 39 kb DNA fragment, located 10 kb upstream of the neighbouring interleukin genes IL21 and IL2. The frequency of the deletion allele was 0.81 in the available cases and 0.25 in a random sample of the Kooiker dog breed. Leukocytes of affected, untreated dogs that were homozygous for the deletion overexpress IL21 and IL2 upon stimulation with mitogens. We suggest that elements located 10-49 kb upstream of the IL21/IL2 locus play an important role in the regulation of the canine genes and that deletion of these elements is a risk factor for polymyositis in Kooiker dogs. Postulating causality, the penetrance of the disease phenotype was estimated at 10-20% for homozygous dogs and 0.5-2% for dogs that were heterozygous for the deletion. Our results suggest that distant variants upstream of IL21 could also be important for human autoimmune diseases that have been found to be associated with the IL21/IL2 chromosome region.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"21 1","pages":"e1011538"},"PeriodicalIF":4.0,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142923655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fitness landscapes of human microsatellites.","authors":"Ryan J Haasl, Bret A Payseur","doi":"10.1371/journal.pgen.1011524","DOIUrl":"https://doi.org/10.1371/journal.pgen.1011524","url":null,"abstract":"<p><p>Advances in DNA sequencing technology and computation now enable genome-wide scans for natural selection to be conducted on unprecedented scales. By examining patterns of sequence variation among individuals, biologists are identifying genes and variants that affect fitness. Despite this progress, most population genetic methods for characterizing selection assume that variants mutate in a simple manner and at a low rate. Because these assumptions are violated by repetitive sequences, selection remains uncharacterized for an appreciable percentage of the genome. To meet this challenge, we focus on microsatellites, repetitive variants that mutate orders of magnitude faster than single nucleotide variants, can harbor substantial variation, and are known to influence biological function in some cases. We introduce four general models of natural selection that are each characterized by just two parameters, are easily simulated, and are specifically designed for microsatellites. Using a random forests approach to approximate Bayesian computation, we fit these models to carefully chosen microsatellites genotyped in 200 humans from a diverse collection of eight populations. Altogether, we reconstruct detailed fitness landscapes for 43 microsatellites we classify as targets of selection. Microsatellite fitness surfaces are diverse, including a range of selection strengths, contributions from dominance, and variation in the number and size of optimal alleles. Microsatellites that are subject to selection include loci known to cause trinucleotide expansion disorders and modulate gene expression, as well as intergenic loci with no obvious function. The heterogeneity in fitness landscapes we report suggests that genome-scale analyses like those used to assess selection targeting single nucleotide variants run the risk of oversimplifying the evolutionary dynamics of microsatellites. Moreover, our fitness landscapes provide a valuable visualization of the selective dynamics navigated by microsatellites.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"20 12","pages":"e1011524"},"PeriodicalIF":4.0,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142957345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory KIRs decrease HLA class II-mediated protection in Type 1 Diabetes.","authors":"Laura Mora-Bitria, Bisrat J Debebe, Kelly L Miners, Kristin Ladell, Charandeep Kaur, James A Traherne, Wei Jiang, David A Price, Linda Hadcocks, Nicholas A R McQuibban, John Trowsdale, F Susan Wong, Nikolas Pontikos, Christoph Niederalt, Becca Asquith","doi":"10.1371/journal.pgen.1011456","DOIUrl":"https://doi.org/10.1371/journal.pgen.1011456","url":null,"abstract":"<p><p>Inhibitory killer cell immunoglobulin-like receptors (iKIRs) are a family of inhibitory receptors that are expressed by natural killer (NK) cells and late-stage differentiated T cells. There is accumulating evidence that iKIRs regulate T cell-mediated immunity. Recently, we reported that T cell-mediated control was enhanced by iKIRs in chronic viral infections. We hypothesized that in the context of autoimmunity, where an enhanced T cell response might be considered detrimental, iKIRs would have an opposite effect. We studied Type 1 diabetes (T1D) as a paradigmatic example of autoimmunity. In T1D, variation in the Human Leucocyte Antigen (HLA) genes explains up to 50% of the genetic risk, indicating that T cells have a major role in T1D etiopathogenesis. To investigate if iKIRs affect this T cell response we asked whether HLA associations were modified by iKIR genes. We conducted an immunogenetic analysis of a case-control T1D dataset (N = 11,961) and found that iKIR genes, in the presence of genes encoding their ligands, have a consistent and significant effect on protective HLA class II genetic associations. Our results were validated in an independent data set. We conclude that iKIRs significantly decrease HLA class II protective associations and suggest that iKIRs regulate CD4+ T cell responses in T1D.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"20 12","pages":"e1011456"},"PeriodicalIF":4.0,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142899717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RcsF-independent mechanisms of signaling within the Rcs phosphorelay.","authors":"Anushya Petchiappan, Nadim Majdalani, Erin Wall, Susan Gottesman","doi":"10.1371/journal.pgen.1011408","DOIUrl":"https://doi.org/10.1371/journal.pgen.1011408","url":null,"abstract":"<p><p>The Rcs (regulator of capsule synthesis) phosphorelay is a conserved cell envelope stress response mechanism in enterobacteria. It responds to perturbations at the cell surface and the peptidoglycan layer from a variety of sources, including antimicrobial peptides, beta-lactams, and changes in osmolarity. RcsF, an outer membrane lipoprotein, is the sensor for this pathway and activates the phosphorelay by interacting with an inner membrane protein IgaA. IgaA is essential; it negatively regulates the signaling by interacting with the phosphotransferase RcsD. We previously showed that RcsF-dependent signaling does not require the periplasmic domain of the histidine kinase RcsC and identified a dominant negative mutant of RcsD that can block signaling via increased interactions with IgaA. However, how the inducing signals are sensed and how signal is transduced to activate the transcription of the Rcs regulon remains unclear. In this study, we investigated how the Rcs cascade functions without its only known sensor, RcsF, and characterized the underlying mechanisms for three distinct RcsF-independent inducers. Previous reports showed that Rcs activity can be induced in the absence of RcsF by a loss of function mutation in the periplasmic oxidoreductase DsbA or by overexpression of the DnaK cochaperone DjlA. We identified an inner membrane protein, DrpB, as a multicopy RcsF-independent Rcs activator in E. coli. The loss of the periplasmic oxidoreductase DsbA and the overexpression of the DnaK cochaperone DjlA each trigger the Rcs cascade in the absence of RcsF by weakening IgaA-RcsD interactions in different ways. In contrast, the cell-division associated protein DrpB uniquely requires the RcsC periplasmic domain for activation; this domain is not needed for RcsF-dependent signaling. This suggests the possibility that the RcsC periplasmic domain acts as a sensor for some Rcs signals. Overall, the results add new understanding to how this complex phosphorelay can be activated by diverse mechanisms.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"20 12","pages":"e1011408"},"PeriodicalIF":4.0,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142899683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decreased Hsp90 activity protects against TDP-43 neurotoxicity in a C. elegans model of amyotrophic lateral sclerosis.","authors":"Laura Garcia-Toscano, Heather N Currey, Joshua C Hincks, Jade G Stair, Nicolas J Lehrbach, Nicole F Liachko","doi":"10.1371/journal.pgen.1011518","DOIUrl":"10.1371/journal.pgen.1011518","url":null,"abstract":"<p><p>Neuronal inclusions of hyperphosphorylated TDP-43 are hallmarks of disease for most patients with amyotrophic lateral sclerosis (ALS). Mutations in TARDBP, the gene coding for TDP-43, can cause some cases of familial inherited ALS (fALS), indicating dysfunction of TDP-43 drives disease. Aggregated, phosphorylated TDP-43 may contribute to disease phenotypes; alternatively, TDP-43 aggregation may be a protective cellular response sequestering toxic protein away from the rest of the cell. The heat shock responsive chaperone Hsp90 has been shown to interact with TDP-43 and stabilize its normal conformation; however, it is not known whether this interaction contributes to neurotoxicity in vivo. Using a C. elegans model of fALS mutant TDP-43 proteinopathy, we find that loss of function of HSP-90 protects against TDP-43 neurotoxicity and subsequent neurodegeneration in adult animals. This protection is accompanied by a decrease in both total and phosphorylated TDP-43 protein. We also find that hsp-90 mutation or inhibition upregulates key stress responsive heat shock pathway gene expression, including hsp-70 and hsp-16.1, and we demonstrate that normal levels of hsp-16.1 are required for hsp-90 mutation effects on TDP-43. We also observe that the neuroprotective effect due to HSP-90 dysfunction does not involve direct regulation of proteasome activity in C. elegans. Our data demonstrate for the first time that Hsp90 chaperone activity contributes to adverse outcomes in TDP-43 proteinopathies in vivo using a whole animal model of ALS.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"20 12","pages":"e1011518"},"PeriodicalIF":4.0,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11709271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142899709","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}