Genetics最新文献

{"title":"Error rates in QST-FST comparisons depend on genetic architecture and estimation procedures.","authors":"Junjian J Liu, Michael D Edge","doi":"10.1093/genetics/iyaf034","DOIUrl":"10.1093/genetics/iyaf034","url":null,"abstract":"<p><p>Genetic and phenotypic variation among populations is one of the fundamental subjects of evolutionary genetics. One question that arises often in data on natural populations is whether differentiation among populations on a particular trait might be caused in part by natural selection. For the past several decades, researchers have used QST-FST approaches to compare the amount of trait differentiation among populations on one or more traits (measured by the statistic QST) with differentiation on genome-wide genetic variants (measured by FST). Theory says that under neutrality, FST and QST should be approximately equal in expectation, so QST values much larger than FST are consistent with local adaptation driving subpopulations' trait values apart, and QST values much smaller than FST are consistent with stabilizing selection on similar optima. At the same time, investigators have differed in their definitions of genome-wide FST (such as \"ratio of averages\" vs. \"average of ratios\" versions of FST) and in their definitions of the variance components in QST. Here, we show that these details matter. Different versions of FST and QST have different interpretations in terms of coalescence time, and comparing incompatible statistics can lead to elevated type I error rates, with some choices leading to type I error rates near one when the nominal rate is 5%. We conduct simulations under varying genetic architectures and forms of population structure and show how they affect the distribution of QST. When many loci influence the trait, our simulations support procedures grounded in a coalescent-based framework for neutral phenotypic differentiation.</p>","PeriodicalId":48925,"journal":{"name":"Genetics","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143558494","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}

{"title":"Suppression of meiotic crossovers in pericentromeric heterochromatin requires synaptonemal complex and meiotic recombination factors in Drosophila melanogaster.","authors":"Nila M Pazhayam, Sasha Sagar, Jeff Sekelsky","doi":"10.1093/genetics/iyaf029","DOIUrl":"10.1093/genetics/iyaf029","url":null,"abstract":"<p><p>The centromere effect (CE) is a meiotic phenomenon that ensures meiotic crossover suppression in pericentromeric regions. Despite being a critical safeguard against nondisjunction, the mechanisms behind the CE remain unknown. Previous studies found that different regions of the Drosophila pericentromere, encompassing proximal euchromatin, beta, and alpha heterochromatin, undergo varying levels of crossover suppression, raising the question of whether distinct mechanisms establish the CE in different regions. We asked whether different pericentromeric regions respond differently to mutations that impair features that may play a role in the CE. In flies with a mutation that affects the synaptonemal complex (SC), a structure that is hypothesized to have roles in recombination and crossover patterning, we observed a redistribution of pericentromeric crossovers from proximal euchromatin towards beta heterochromatin but not alpha heterochromatin, indicating a role for the SC in suppressing crossovers in beta heterochromatin. In flies mutant for mei-218 or rec, which encode components of a critical pro-crossover complex, there was a more extreme redistribution of pericentromeric crossovers towards both beta and alpha heterochromatin, suggesting an important role for these meiotic recombination factors in suppressing heterochromatic crossovers. We mapped crossovers in flies mutant for Su(var)3-9, which encodes histone H3-lysine-9 methyltransferase. Although we expected strong alleviation of crossover suppression in heterochromatin, no changes in pericentromeric crossover distribution were observed in this mutant, indicating that this vital heterochromatin factor is dispensable for preventing crossovers in heterochromatin. Thus, in Drosophila. melanogaster the meiotic machinery seems to play a more significant role in suppressing centromere-proximal crossovers than chromatin state.</p>","PeriodicalId":48925,"journal":{"name":"Genetics","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143494317","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}

{"title":"Robust sex determination in the Caenorhabditis nigoni germ line.","authors":"Jonathan P Harbin, Yongquan Shen, Shin-Yi Lin, Kevin Kemper, Eric S Haag, Erich M Schwarz, Ronald E Ellis","doi":"10.1093/genetics/iyae207","DOIUrl":"10.1093/genetics/iyae207","url":null,"abstract":"<p><p>Sexual characteristics and reproductive systems are dynamic traits in many taxa, but the developmental modifications that allow change and innovation are largely unknown. A leading model for this process is the evolution of self-fertile hermaphrodites from male/female ancestors. However, these studies require direct analysis of sex determination in male/female species, as well as in the hermaphroditic species that are related to them. In Caenorhabditis nematodes, this has only become possible recently, with the discovery of new species. Here, we use gene editing to characterize major sex determination genes in Caenorhabditis nigoni, a sister to the widely studied hermaphroditic species Caenorhabditis briggsae. These 2 species are close enough to mate and form partially fertile hybrids. First, we find that tra-1 functions as the master regulator of sex in C. nigoni, in both the soma and the germ line. Surprisingly, these mutants make only sperm, in contrast to tra-1 mutants in related hermaphroditic species. Moreover, the XX mutants display a unique defect in somatic gonad development that is not seen elsewhere in the genus. Second, the fem-3 gene acts upstream of tra-1 in C. nigoni, and the mutants are females, unlike in the sister species C. briggsae, where they develop as hermaphrodites. This result points to a divergence in the role of fem-3 in the germ line of these species. Third, tra-2 encodes a transmembrane receptor that acts upstream of fem-3 in C. nigoni. Outside of the germ line, tra-2 mutations in all species cause a similar pattern of partial masculinization. However, heterozygosity for tra-2 does not alter germ cell fates in C. nigoni, as it can in sensitized backgrounds of 2 hermaphroditic species of Caenorhabditis. Finally, the epistatic relationships point to a simple, linear germline pathway in which tra-2 regulates fem-3 which regulates tra-1, unlike the more complex relationships seen in hermaphrodite germ cell development. Taking these results together, the regulation of sex determination is more robust and streamlined in the male/female species C. nigoni than in related species that make self-fertile hermaphrodites, a conclusion supported by studies of interspecies hybrids using sex determination mutations. Thus, we infer that the origin of self-fertility not only required mutations that activated the spermatogenesis program in XX germ lines, but prior to these there must have been mutations that decanalized the sex determination process, allowing for subsequent changes to germ cell fates.</p>","PeriodicalId":48925,"journal":{"name":"Genetics","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142814683","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}

{"title":"Neuron-specific repression of alternative splicing by the conserved CELF protein UNC-75 in Caenorhabditis elegans.","authors":"Pallavi Pilaka-Akella, Nour H Sadek, Daniel Fusca, Asher D Cutter, John A Calarco","doi":"10.1093/genetics/iyaf025","DOIUrl":"10.1093/genetics/iyaf025","url":null,"abstract":"<p><p>Tissue-regulated alternative exons are dictated by the interplay between cis-elements and trans-regulatory factors such as RNA-binding proteins (RBPs). Despite extensive research on splicing regulation, the full repertoire of these cis and trans features and their evolutionary dynamics across species are yet to be fully characterized. Members of the CUG-binding protein and ETR-like family (CELF) of RBPs are known to play a key role in the regulation of tissue-biased splicing patterns, and when mutated, these proteins have been implicated in a number of neurological and muscular disorders. In this study, we sought to characterize specific mechanisms that drive tissue-specific splicing in vivo of a model switch-like exon regulated by the neuronal-enriched CELF ortholog in Caenorhabditis elegans, UNC-75. Using sequence alignments, we identified deeply conserved intronic UNC-75 binding motifs overlapping the 5' splice site and upstream of the 3' splice site, flanking a strongly neural-repressed alternative exon in the Zonula Occludens gene zoo-1. We confirmed that loss of UNC-75 or mutations in either of these cis-elements lead to substantial de-repression of the alternative exon in neurons. Moreover, mis-expression of UNC-75 in muscle cells is sufficient to induce the neuron-like robust skipping of this alternative exon. Lastly, we demonstrate that overlapping an UNC-75 motif within a heterologous 5' splice site leads to increased skipping of the adjacent alternative exon in an unrelated splicing event. Together, we have demonstrated that a specific configuration and combination of cis elements bound by this important family of RBPs can achieve robust splicing outcomes in vivo.</p>","PeriodicalId":48925,"journal":{"name":"Genetics","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143587824","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}

{"title":"Epistasis and cryptic QTL identified using modified bulk segregant analysis of copper resistance in budding yeast.","authors":"Cassandra Buzby, Yevgeniy Plavskin, Federica M O Sartori, Qiange Tong, Janessa K Vail, Mark L Siegal","doi":"10.1093/genetics/iyaf026","DOIUrl":"10.1093/genetics/iyaf026","url":null,"abstract":"<p><p>The contributions of genetic interactions to natural trait variation are challenging to estimate experimentally, as current approaches for detecting epistasis are often underpowered. Powerful mapping approaches such as bulk segregant analysis (BSA), wherein individuals with extreme phenotypes are pooled for genotyping, obscure epistasis by averaging over genotype combinations. To accurately characterize and quantify epistasis underlying natural trait variation, we have engineered strains of the budding yeast Saccharomyces cerevisiae to enable crosses where one parent's chromosome is fixed while the rest of the chromosomes segregate. These crosses allow us to use BSA to identify quantitative trait loci (QTL) whose effects depend on alleles on the fixed parental chromosome, indicating a genetic interaction with that chromosome. Our method, which we term epic-QTL (for epistatic-with-chromosome QTL) analysis, can thus identify interaction loci with high statistical power. Here, we perform epic-QTL analysis of copper resistance with chromosome I or VIII fixed in a cross between divergent naturally derived strains. We find 7 loci that interact significantly with chromosome VIII and none that interact with chromosome I, the smallest of the 16 budding yeast chromosomes. Each of the 7 interactions alters the magnitude, rather than the direction, of an additive QTL effect. We also show that fixation of one source of variation-in this case, chromosome VIII, which contains the large-effect QTL mapping to CUP1-increases power to detect the contributions of other loci to trait differences.</p>","PeriodicalId":48925,"journal":{"name":"Genetics","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143484245","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}

{"title":"Complex determinants of R-loop formation at transposable elements and major DNA satellites.","authors":"Timothy J Stanek, Adam Kneebone, Matthew A Lawlor, Weihuan Cao, Christopher E Ellison","doi":"10.1093/genetics/iyaf035","DOIUrl":"10.1093/genetics/iyaf035","url":null,"abstract":"<p><p>Aberrant activation of transposable elements (TEs) has been a well-documented source of genomic instability and disease, stemming from their insertion into genes and their imposition of epigenetic effects on nearby loci. However, the extent to which their disruptive effects involve concomitant or subsequent formation of DNA:RNA hybrids (R-loops) remains unknown. Here, we used DNA:RNA immunoprecipitation followed by high-throughput sequencing (DRIP-seq) to map the R-loop profiles of TEs and satellites in Drosophila melanogaster ovaries in control and rhino knockout flies, where dozens of TE families are derepressed. We observe that R-loops form primarily in LTR retrotransposons that carry A/T-rich sequence motifs, which are known to favor R-loop formation at genes in Drosophila and other species. We also report evidence of R-loop formation at 11 of 14 highly abundant D. melanogaster DNA satellites. R-loop formation is positively correlated with expression level for both TEs and satellites; however, neither sequence content nor expression fully explain which repeat families form R-loops, suggesting other factors are at play. Finally, by analyzing population frequencies of R-loop-forming TEs, we present evidence that TE copies with high R-loop signal may be under stronger negative selection, which suggests that R-loop formation by TEs may be deleterious to their host. Collectively, these results provide insight into the determinants of R-loop formation at repetitive elements.</p>","PeriodicalId":48925,"journal":{"name":"Genetics","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143558490","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}

{"title":"A Bayesian approach to correcting the attenuation bias of regression using polygenic risk score.","authors":"Geyu Zhou, Xinyue Qie, Hongyu Zhao","doi":"10.1093/genetics/iyaf018","DOIUrl":"10.1093/genetics/iyaf018","url":null,"abstract":"<p><p>Polygenic risk score has become increasingly popular for predicting the value of complex traits. In many settings, polygenic risk score is used as a covariate in regression analysis to study the association between different phenotypes. However, measurement error in polygenic risk score causes attenuation bias in the estimation of regression coefficients. In this paper, we employ a Bayesian approach to accounting for the measurement error of polygenic risk score and correcting the attenuation bias in linear and logistic regression. Through simulation, we show that our approach is able to obtain approximately unbiased estimation of coefficients and credible intervals with correct coverage probability. We also empirically compare our Bayesian measurement error model with the conventional regression model by analyzing real traits in the UK Biobank. The results demonstrate the effectiveness of our approach as it significantly reduces the error in coefficient estimates.</p>","PeriodicalId":48925,"journal":{"name":"Genetics","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143075983","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":"The homie insulator has sub-elements with different insulating and long-range pairing properties.","authors":"Miki Fujioka, Wenfan Ke, Paul Schedl, James B Jaynes","doi":"10.1093/genetics/iyaf032","DOIUrl":"10.1093/genetics/iyaf032","url":null,"abstract":"<p><p>Chromatin insulators are major determinants of chromosome architecture. Specific architectures induced by insulators profoundly influence nuclear processes, including how enhancers and promoters interact over long distances and between homologous chromosomes. Insulators can pair with copies of themselves in trans to facilitate homolog pairing. They can also pair with other insulators, sometimes with great specificity, inducing long-range chromosomal loops. Contrary to their canonical function of enhancer blocking, these loops can bring distant enhancers and promoters together to activate gene expression, while at the same time blocking other interactions in cis. The details of these effects depend on the choice of pairing partner, and on the orientation specificity of pairing, implicating the 3D architecture as a major functional determinant. Here, we dissect the homie insulator from the Drosophila even skipped (eve) locus, to understand its substructure. We test pairing function based on homie-carrying transgenes interacting with endogenous eve. The assay is sensitive to both pairing strength and orientation. Using this assay, we found that a Su(Hw) binding site in homie is required for efficient long-range interaction, although some activity remains without it. This binding site also contributes to the canonical insulator activities of enhancer blocking and barrier function. Based on this and other results from our functional dissection, each of the canonical insulator activities, chromosomal loop formation, enhancer blocking, and barrier activity, are partially separable. Our results show the complexity inherent in insulator functions, which can be provided by an array of different proteins with both shared and distinct properties.</p>","PeriodicalId":48925,"journal":{"name":"Genetics","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143505255","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}

{"title":"The Rac1 homolog CED-10 is a component of the MES-1/SRC-1 pathway for asymmetric division of the Caenorhabditis elegans EMS blastomere.","authors":"Helen Lamb, McKenzi Fernholz, Małgorzata J Liro, Krista M Myles, Holly Anderson, Lesilee S Rose","doi":"10.1093/genetics/iyaf020","DOIUrl":"10.1093/genetics/iyaf020","url":null,"abstract":"<p><p>Asymmetric cell division is essential for the creation of cell types with different identities and functions. The endomesodermal precursor cell (EMS) of the 4-cell Caenorhabditis elegans embryo undergoes an asymmetric division in response to partially redundant signaling pathways. One pathway involves a Wnt signal from the neighboring P2 cell, while the other pathway is defined by the receptor-like MES-1 transmembrane protein localized at the EMS-P2 cell contact and the cytoplasmic kinase SRC-1. In response to these signals, the EMS nuclear-centrosome complex rotates, so that the spindle forms on the anterior-posterior axis; after division, the daughter cell contacting P2 becomes the endodermal precursor cell. Here, we identify the Rac1 homolog CED-10 as a new component of the MES-1/SRC-1 pathway. Loss of CED-10 affects both spindle positioning and endoderm specification in the EMS cell. SRC-1 dependent phosphorylation at the EMS-P2 contact is reduced. However, the asymmetric division of the P2 cell, which is also MES-1 and SRC-1 dependent, appears normal in ced-10 mutants. These and other results suggest that CED-10 acts upstream of, or at the level of, SRC-1 activity in the EMS cell. In addition, we find that the branched actin regulator ARX-2 is enriched at the EMS-P2 cell contact site, in a CED-10-dependent manner. Loss of ARX-2 results in EMS spindle orientation defects, suggesting that CED-10 acts through branched actin to promote spindle orientation in the EMS cell.</p>","PeriodicalId":48925,"journal":{"name":"Genetics","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143075984","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}

{"title":"Multiple DNA repair pathways prevent acetaldehyde-induced mutagenesis in yeast.","authors":"Latarsha Porcher, Sriram Vijayraghavan, Yashvi Patel, Samuel Becker, Thomas Blouin, James McCollum, Piotr A Mieczkowski, Natalie Saini","doi":"10.1093/genetics/iyae213","DOIUrl":"10.1093/genetics/iyae213","url":null,"abstract":"<p><p>Acetaldehyde is the primary metabolite of alcohol and is present in many environmental sources, including tobacco smoke. Acetaldehyde is genotoxic, whereby it can form DNA adducts and lead to mutagenesis. Individuals with defects in acetaldehyde clearance pathways have increased susceptibility to alcohol-associated cancers. Moreover, a mutation signature specific to acetaldehyde exposure is widespread in alcohol- and smoking-associated cancers. However, the pathways that repair acetaldehyde-induced DNA damage and thus prevent mutagenesis are vaguely understood. Here, we used Saccharomyces cerevisiae to delete genes in each of the major DNA repair pathways to identify those that alter acetaldehyde-induced mutagenesis. We observed that loss of functional nucleotide excision repair had the largest effect on acetaldehyde mutagenesis. In addition, base excision repair and DNA protein crosslink repair pathways were involved in modulating acetaldehyde mutagenesis, while mismatch repair, homologous recombination, and postreplication repair are dispensable for acetaldehyde mutagenesis. Acetaldehyde-induced mutations in a nucleotide excision repair-deficient (Δrad1) background were dependent on translesion synthesis and DNA interstrand crosslink repair. Moreover, whole-genome sequencing of the mutated isolates demonstrated an increase in C→A changes coupled with an enrichment of gCn→A changes, which is diagnostic of acetaldehyde exposure in yeast and in human cancers. Finally, downregulation of the leading strand replicative polymerase Pol epsilon, but not the lagging strand polymerase, resulted in increased acetaldehyde mutagenesis, indicating that lesions are likely formed on the leading strand. Our findings demonstrate that multiple DNA repair pathways coordinate to prevent acetaldehyde-induced mutagenesis.</p>","PeriodicalId":48925,"journal":{"name":"Genetics","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142873069","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}