PLoS Genetics最新文献

{"title":"ER-to-Golgi transport machinery promotes the excessive cargo-triggered unfolded protein response in C. elegans.","authors":"Liying Guan, Tong Zhang, Zhigao Zhan, Yingchun Wang, Xun Huang, Mei Ding","doi":"10.1371/journal.pgen.1012301","DOIUrl":"10.1371/journal.pgen.1012301","url":null,"abstract":"<p><p>Disruption of endoplasmic reticulum (ER) homeostasis activates the unfolded protein response (UPR) to restore proteostasis. Although defects in the secretory machinery can induce ER stress, whether specific trafficking components actively couple cargo handling to UPR signaling remains unclear. Here, using Caenorhabditis elegans genetics, imaging, and biochemical assays, we show that neuronal overexpression of the gap junction protein UNC-9 cell-autonomously activates the IRE-1-XBP-1 branch of the ER UPR. Loss of the early secretory pathway proteins ERGI-2 or ERGI-3 suppresses this response and disrupts UNC-9 localization, revealing functions for these proteins that extend beyond cargo trafficking. ERGI-2 and ERGI-3 interact with both UNC-9 and the ER chaperone HSP-4/BiP, suggesting that they couple the handling of excessive UNC-9 to UPR activation. This requirement is cargo-selective: ERGI-2 and ERGI-3 are dispensable for UPR activation induced by overexpression of another innexin, UNC-7, or unrelated proteins. Moreover, activation of the IRE-1-XBP-1 pathway reduces abnormal UNC-9 accumulation in ergi-2 and ergi-3 mutants. Together, our findings identify ER-to-Golgi trafficking proteins as cargo-selective regulators that link secretory-pathway demand to adaptive UPR.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 9","pages":"e1012301"},"PeriodicalIF":3.9,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13568704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148913417","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":"OsDUF1223 negatively regulates seedling drought tolerance and modulates nitrate-dependent root growth in rice.","authors":"Xiulin Zhao, Ziyi Wang, Mingfei Chen, Lingxiang Lu, Hui Lin, Xiaofei Zan, Xiaomei Jia, Xiaoying Ye, Rongjun Chen, Jianqing Zhu, Jun Zhu, Lihua Li","doi":"10.1371/journal.pgen.1012295","DOIUrl":"10.1371/journal.pgen.1012295","url":null,"abstract":"<p><p>Rice (Oryza sativa L.) is a major staple food crop worldwide. Drought stress induced by extreme weather severely limits its growth and yield. Proteins containing domains of unknown function (DUF) play important roles in plant stress responses, but their regulatory mechanisms remain largely unclear. In this study, we demonstrate that the plasma membrane-localized protein OsDUF1223 functions as a negative regulator of drought tolerance in rice seedlings. Under drought stress, OsDUF1223-overexpressing lines exhibited lower survival rates, higher water loss rates, and reduced antioxidant enzyme activities and osmolyte accumulation. Transcriptomic and physiological analyses revealed that OsDUF1223 modulates drought responses through ABA signaling and nitrogen response pathways. Collectively, this study elucidates that OsDUF1223 regulates drought tolerance at the seedling stage in rice through functional association with the ABA and nitrogen signaling pathways, thereby providing a candidate gene resource for the genetic improvement of drought tolerance in rice.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 9","pages":"e1012295"},"PeriodicalIF":3.9,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888614","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":"Post-transcriptional regulation of Profilin-2 by microRNAs and RNA-binding proteins forms a critical regulatory node for early embryonic cell fate decisions.","authors":"Carolyn Sangokoya, Isabella R Rosso, Rana Ghandehari-Alavijeh, Robert Blelloch","doi":"10.1371/journal.pgen.1012279","DOIUrl":"10.1371/journal.pgen.1012279","url":null,"abstract":"<p><p>Post-transcriptional control by RNA binding proteins (RBPs) and microRNAs play central roles in mRNA stability and translation, yet how RBPs and microRNAs coordinate in developmental time to regulate cell fate remains poorly understood. Here, we demonstrate that post-transcriptional regulation of the Profilin 2 (Pfn2) transcript is essential for differentiation of embryonic stem cells (ESCs) into the primary germ layer lineages. The Pfn2 3'untranslated region has both an Iron Regulatory Protein binding site (IRE) and a nearby binding site for ESC enriched microRNAs. Deletion of this microRNA site leads to increased PFN2 and reduced FGF signaling during pluripotency transition prior to germ layer formation. In contrast, deletion of the IRE leads to decreased PFN2, a Wnt signaling defect, reduced nuclear beta-catenin, and a subsequent block in mesendodermal lineages during early germ layer formation. We further find that loss of the IRE site results in a cell autonomous defect in Wnt signaling and mesendodermal differentiation. The IRE site acts to stabilize beta-catenin, as disruption of the site leads to reduced nuclear beta-catenin levels. Together, these findings reveal the Pfn2 microRNA-IRE regulatory axis as a critical post-transcriptional regulatory node governing the switch from pluripotency to somatic differentiation.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 9","pages":"e1012279"},"PeriodicalIF":3.9,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13537575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148882421","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":"The SigD regulon of Mycobacterium abscessus determines cell envelope composition and antibiotic susceptibility.","authors":"Sean R Jones, Kelly Maune, Kelley Hurst-Hess, Pallavi Ghosh","doi":"10.1371/journal.pgen.1012286","DOIUrl":"10.1371/journal.pgen.1012286","url":null,"abstract":"<p><p>A major determinant of the exceptional intrinsic resistance of M. abscessus is the lipid-rich cell envelope, yet the regulatory systems that remodel envelope-associated pathways remain poorly defined. Here, we determine the σD regulon in M. abscessus and establish its role in cell envelope homeostasis and intrinsic resistance to hydrophobic antibiotics. RNA-Seq analysis of a MabΔsigD mutant identified 447 differentially expressed genes, while ChIP-Seq mapped 72 σD binding sites and defined a conserved promoter motif (GTAACA/G-N16-CGAT). Using a combination of σD binding, motif orientation and expression data, we identified a core set of directly regulated genes, distinct from what was previously observed in M. tuberculosis, many of which encode proteins involved in envelope-associated functions. These include loci involved in trehalose polyphleate (TPP) biosynthesis, the antigen 85 complex and peptidoglycan remodeling enzymes. Deletion of sigD resulted in a significant reduction in TPPs in the cell envelope and an increase in ethidium bromide accumulation. Consistent with these changes, loss of σD selectively sensitized M. abscessus to hydrophobic antibiotics, including rifampicin and tigecycline. Deletion of mmpL10, which is required for transport of TPP precursors, recapitulated the drug sensitivity of MabΔsigD, implicating envelope composition as a key effector of the phenotype. Expression of the σD regulon further increased during starvation and in response to SDS, isoniazid, and ethambutol, mediated by degradation of RsdA, consistent with a role in stress-responsive envelope adaptation. Together, these findings demonstrate σD is active during logarithmic growth in rich media where it regulates the expression of envelope-associated genes that influence envelope permeability and basal level susceptibility to hydrophobic antibiotics; its activity further increases in response to cell envelope stress, presumably promoting envelope remodeling to counteract damage.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 9","pages":"e1012286"},"PeriodicalIF":3.9,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13537577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148882388","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":"Multi-organ single-cell transcriptomic atlas identifies QrIAA14 as a candidate negative regulator of adventitious root development in Quercus robur.","authors":"Wenkai Hui, Jiayue Li, Hao Li, Hongyi Wu, Yi He, Shuangying Yang, Xiong Huang, Hanbo Yang, Gang Chen, Peng Zhu, Xiaohong Chen, Xingcui Xiao, Yu Zhong, Zhenfeng Xu, Fang He","doi":"10.1371/journal.pgen.1012300","DOIUrl":"10.1371/journal.pgen.1012300","url":null,"abstract":"<p><p>Plant organ development involves coordinated cell fate transitions across multiple tissues, yet the cellular programs underlying organ-specific differentiation in woody plants remain poorly understood, particularly the mechanisms limiting efficient root development during vegetative propagation of oak species. Here, we generated a comprehensive single-cell transcriptomic landscape of leaf, stem, and root tissues of Quercus robur to resolve developmental trajectories at cellular resolution. A total of 41,471 high-quality cells were classified into 30 distinct clusters, enabling the identification of major cell types and organ-specific transcriptional features across three vegetative organs. Pseudotime analyses exhibited the developmental programs related to guard cell differentiation in leaves, vascular formation in stems, and root tissue development. Additionally, combining scRNA-seq, bulk transcriptome profiling, and phytohormone investigations, we identified auxin signaling as an important regulator during adventitious root development process. Notably, QrIAA14-1, an IAA14 homolog, was preferential enrichment in root hair, near-root hair cells and root cap along root developmental trajectories, which was further supported by RT-qPCR and in situ hybridization assays. Furthermore, the overexpression of QrIAA14-1 significantly inhibited oak root elongation, resulting in around 64.46% reduction in adventitious root length compared with control plants, providing mechanistic insight into the limitations of root development in oak. Together, this study provides the first high-resolution single-cell atlas of cellular organization and developmental dynamics across oak vegetative organs and identifies the candidate regulator genes associated with root development, offering new insights into the regulatory mechanisms of woody plant root regeneration and clonal propagation.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 9","pages":"e1012300"},"PeriodicalIF":3.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148875958","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":"Abdominal-B regulates the male seminal fluid transferome and new fecundity factors required for sperm sex peptide binding.","authors":"Kathrin Steck, Lina Verbakel, Peter Kerwin, Vladimir Trajanovikj, Katarzyna Kjøge, Jan J Enghild, Anne C von Philipsborn","doi":"10.1371/journal.pgen.1012298","DOIUrl":"10.1371/journal.pgen.1012298","url":null,"abstract":"<p><p>Seminal fluid proteins determine reproductive success in a wide range of animals. In the Drosophila male accessory gland, seminal fluid is mainly produced by two cell types, a majority of main cells and a small number of secondary cells that possess a specialized secretory apparatus with unusually enlarged dense core granule vesicles. Loss of Abdominal-B expression from secondary cells in the enhancer mutant iab-6cocu disrupts their transcriptional and secretory identity. Consequently, mutant males fail to induce the long-term post-mating response in females, which is characterized by a loss of receptivity and sustained egg laying. Here, we determine how secondary cells shape the seminal transferome and the female response by assessing iab-6cocu male accessory gland and female mate reproductive tract proteomes. We find downregulation of seminal fluid proteins that constitute a signaling network enabling sperm binding and the sustained action of the key regulator Sex Peptide. We identify two new Sex Peptide network proteins crucial for female fecundity, Cornutus (CG1701) and Hanrej (CG42564). Cornutus is required for mating dependent dense core granule vesicle release, providing a link between the products of these compartments and the female long-term post-mating response. Our data highlights the importance of secondary cell signaling and secretion for overall seminal fluid composition and Sex Peptide network function as well as the interdependence of main and secondary cells and their secretory products, advancing the general understanding of how seminal fluid signaling pathways modulate female physiology, sperm use and offspring production.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 9","pages":"e1012298"},"PeriodicalIF":3.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557496/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148875658","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":"Characterization of METTL3/14-mediated m6A modification in human transcriptome using Nanopore direct RNA sequencing.","authors":"Emily Kurtyan, Andrew J Stein, Kelly J Abdalla, Zhangerjiao Yuan, Miten Jain, Fadia Ibrahim","doi":"10.1371/journal.pgen.1012278","DOIUrl":"10.1371/journal.pgen.1012278","url":null,"abstract":"<p><p>Post-transcriptional RNA modifications modulate diverse aspects of RNA metabolism. N6-methyladenosine (m6A), one of the most abundant internal RNA modifications, is deposited by the core methyltransferase complex, METTL3 and METTL14. Oxford Nanopore Technologies (ONT) platform permits direct, single RNA molecule sequencing while preserving native modifications. However, without rigorous benchmarking, the accuracy and reproducibility of modification detection remain uncertain. Here, we leveraged ONT to comprehensively profile bona fide m6A modifications in cellular RNAs at single-nucleotide resolution by integrating two direct RNA sequencing chemistries (RNA002 and RNA004) with the m6Anet and Dorado modification-detection models. We independently depleted METTL3 and METTL14 in human cells and rigorously validated modification calls through several assays and independent orthogonal methods (GLORI and miCLIP). We find that Dorado detected a higher number of m6A events and enabled simultaneous detection of other RNA modifications (5-methylcytosine, pseudouridine, and inosine). Pairing Dorado with an in vitro transcribed, unmodified control under stringent filtering, we provide compelling evidence supporting a global reduction in m6A sites and stoichiometry within coding sequences and across genes, particularly in highly modified genes and sites, and at consensus DRACH motifs. We report a differential and complex regulation of modified transcripts, accompanied by a global reduction in poly(A) tail length. Notably, METTL3 and METTL14 depletion produced distinct transcript-specific effects, supporting non-redundant roles within the m6A writer complex. Together, our study illustrates a notable advancement of ONT capabilities and establishes a robust transcriptome-wide framework for RNA modification detection, thereby laying the groundwork for exploring the contribution of METTL3/METTL14 to cellular functions and disease.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 9","pages":"e1012278"},"PeriodicalIF":3.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13533388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148875794","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":"Fungal appressoria as mechanochemical organelles for polyurethane degradation.","authors":"Fan Fei, Zhenjie Su, Rui Liu, Rongrong Gao, Chaomin Sun","doi":"10.1371/journal.pgen.1012292","DOIUrl":"10.1371/journal.pgen.1012292","url":null,"abstract":"<p><p>Polyurethane (PU) is a synthetic polymer characterized by highly stable urethane linkages that hinder biological turnover. Although fungi have been implicated in PU degradation, the molecular mechanisms that couple polymer surface sensing to enzymatic depolymerization remain largely undefined. Here we show that the marine-derived fungus Alternaria alternata FB1 employs a surface-sensing signaling pathway that drives appressorium-mediated degradation of both polyester and polyether PUs. Contact with hydrophobic polymer surfaces rapidly induces melanized appressoria that mechanically penetrate the polymer matrix and promote its oxidative and hydrolytic depolymerization. Integrative transcriptomic analysis and targeted gene disruption identify the mucin-like surface sensor Msb2 as an upstream component of the polyurethane surface-sensing machinery. Loss of Msb2 disrupts MAPK and Ca2+ signaling, impairs appressorium differentiation, and reduces expression of degradative enzymes. Biochemical profiling further reveals multiple urethane-hydrolyzing enzymes that expand the known catalytic repertoire for PU bond cleavage. Together, these findings establish a mechanistic framework linking surface recognition, appressorium development, and polymer degradation, providing insight into how fungi transform recalcitrant polyurethane materials.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 8","pages":"e1012292"},"PeriodicalIF":3.9,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148866399","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":"Convergent latitudinal erosion of circadian systems in a rapidly diversifying order of fishes.","authors":"Daniel B Wright, Yangfan Zhang, Jacob M Daane","doi":"10.1371/journal.pgen.1012287","DOIUrl":"10.1371/journal.pgen.1012287","url":null,"abstract":"<p><p>Biological clocks allow organisms to anticipate cyclical environmental changes, yet in high-latitude or deep-sea habitats, the diel cues that entrain these rhythms are often seasonally diminished or absent. Fishes of the order Perciformes have rapidly diversified across these arrhythmic ecosystems, raising the question of whether changes to circadian rhythms and biological clock genetic architecture are a component of their evolutionary success. Here, we used a comparative genomic approach to investigate patterns of core biological clock gene loss across 96 perciform and five outgroup species. We found widespread and lineage-specific loss in core clock genes, particularly in the convergently evolving polar and deep-sea suborders Notothenioidei and Cottoidei. This trend of clock gene loss was significantly amplified with higher-latitude species. To determine if these genomic signatures reflect a functional loss of rhythmicity, we performed metabolic phenotyping on three notothenioid species. We found a consistent lack of circadian metabolic oscillations during the late austral fall across all notothenioids, including the sub-Antarctic sister lineage to the cryonotothenioid adaptive radiation, Eleginops maclovinus. Experimental data across Perciformes, combined with suborder-wide patterns of gene loss, suggest that a release from circadian constraints occurred early in their diversification, potentially facilitating the repeated expansion of these fishes into polar and deep-sea habitats.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 8","pages":"e1012287"},"PeriodicalIF":3.9,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148866431","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":"A drug repurposing screen reveals dopamine signaling as a candidate therapeutic pathway for PIGA-CDG.","authors":"Miriam C Aziz, Jennie Wilson, Clement Y Chow","doi":"10.1371/journal.pgen.1012294","DOIUrl":"10.1371/journal.pgen.1012294","url":null,"abstract":"<p><p>PIGA-CDG is a congenital disorder of glycosylation caused by pathogenic partial loss-of-function variants in the PIGA gene. PIGA encodes an enzyme responsible for the catalytic transfer of N-acetylglucosamine to phosphatidylinositol during the first step of glycosylphosphatidylinositol anchor biosynthesis. Loss of this enzyme has a widespread phenotypic impact, but primarily results in neurological symptoms including seizures, intellectual disability, and developmental delay. Currently, treatments are limited and focus on symptom management. We developed an eye model of PIGA-CDG that has a reduced eye size. We screened a library of 98% 1,520 FDA/EMA-approved compounds to find drugs that improved the small eye phenotype. This screen revealed numerous drugs that improved eye size, including those that targeted dopamine signaling and cyclooxygenases. Using pharmacological and genetic approaches, we show that modulating dopamine signaling improves the eye size. Genetic inhibition of dopamine 2 receptor signaling and dopamine reuptake improve both the eye model and neurologically relevant PIGA-CDG phenotypes, including seizures and locomotor deficits. We also pharmacologically and genetically validate cyclooxygenase targeting drugs in the eye model. These findings reveal novel biology underlying PIGA-CDG and point towards candidate therapeutic approaches.</p>","PeriodicalId":49007,"journal":{"name":"PLoS Genetics","volume":"22 8","pages":"e1012294"},"PeriodicalIF":3.9,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148866406","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}