Human Genetics最新文献

{"title":"Mitochondrial dysfunction drives metabolic reprogramming in Gitelman syndrome: insights from proteomics and isogenic modeling.","authors":"Honghan Zhang, Wenqian Zhao, Lanxin Ma, Xueli Yang, Jinghua Gao, Xiaoling Liu, Y-G Xie, Ying Hu, Heng Luo, Jian Han","doi":"10.1007/s00439-026-02880-z","DOIUrl":"10.1007/s00439-026-02880-z","url":null,"abstract":"<p><p>Gitelman syndrome (GS) is an autosomal recessive tubulopathy caused by SLC12A3gene mutations. While electrolyte disturbances are well-defined, the systemic metabolic consequences and underlying mechanisms remain unclear. This study investigated whether SLC12A3mutation drives mitochondrial dysfunction and consequent metabolic reprogramming in GS, utilizing a genetically homogeneous founder population with a homozygous SLC12A3p.C421F mutation. We conducted quantitative plasma proteomic analysis (directDIA) in wild-type (WT) and homozygous (HOM) individuals (n = 6/group) and established an isogenic SLC12A3p.C421F homozygous 293T cell model via CRISPR-Cas9. A series of functional assays were performed, including assessment of mitochondrial DNA copy number, membrane potential (JC-1), oxidative stress markers (SOD, MDA, ROS), lipid metabolism (lipid droplets, triglycerides, glycerol, cholesterol), NAD(H)/NADP(H) pools, intracellular ATP levels, enzymatic activities of all five mitochondrial respiratory chain complexes, extracellular acidification rate (ECAR), and expression of key oxidative phosphorylation proteins. Plasma proteomics revealed a significant downregulation of mitochondrial oxidative phosphorylation, TCA cycle, and fatty acid oxidation proteins in HOM individuals. In the cellular model, the mutation recapitulated this signature, showing reduced expression of core respiratory chain subunits (SDHA, UQCRC1, ATP5D). Functionally, HOM cells exhibited impaired activities of respiratory chain complexes I-V, reduced ATP content, and a compensatory increase in glycolytic flux (ECAR). This bioenergetic deficit was accompanied by diminished mtDNA copy number, dissipated mitochondrial membrane potential, elevated oxidative stress, and aberrant lipid metabolism (decreased lipid droplets and triglycerides). Notably, redox cofactor profiling showed a contracted NADP(H) pool alongside an expanded NAD(H) pool. Our integrated multi-omics and functional approach establishes a strong association between the SLC12A3 p.C421F mutation and a state of mitochondrial bioenergetic failure-characterized by impaired oxidative phosphorylation, an ATP deficit, and a compensatory metabolic shift towards glycolysis-in GS. The distinct NAD(H)/NADP(H) imbalance further indicates profound metabolic reprogramming. These findings extend the pathophysiological understanding of GS beyond a pure tubulopathy to a systemic disorder involving mitochondrial dysfunction, offering new mechanistic insights and potential therapeutic targets.</p>","PeriodicalId":13175,"journal":{"name":"Human Genetics","volume":"145 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149016793","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 variation in BDNF is associated with opioid use disorder severity.","authors":"Dara M Kusic, Matthew Salzman, Jessica Heil, Struan F A Grant, Khanh B Trang, Stefan Zajic, Jozef Madzo, Christian Brown, Jaroslav Jelinek, Gennaro Calendo, Roland Schwarting, Jean-Pierre J Issa, Laura B Scheinfeldt","doi":"10.1007/s00439-026-02866-x","DOIUrl":"10.1007/s00439-026-02866-x","url":null,"abstract":"<p><p>As the opioid epidemic continues to challenge local communities in the United States, scientists, clinicians, and community stakeholders are seeking to understand the myriad factors that contribute to misuse in order to develop effective preventions and treatments. Among these efforts is the Camden Opioid Research Initiative (CORI) that aims to identify and characterize genetic and non-genetic risk factors for opioid use disorder (OUD). We explored potential genetic risk factors for OUD severity in four CORI study cohorts (N = 274) using a curated list of 116 candidate single nucleotide polymorphisms (SNPs) previously implicated in opioid dependence. Our results replicate one SNP, rs13306221, in the BDNF gene, as having a significant association with OUD severity. Rs13306221 and a second SNP in strong linkage disequilibrium that is also associated with OUD severity, rs56164415, both lie in an open chromatin domain near the BDNF transcription start site. The rs13306221 genotype associated with increased OUD severity is additionally associated with reduced BDNF expression in lymphoblastoid cell lines consistent with a functional role in BDNF regulation.</p>","PeriodicalId":13175,"journal":{"name":"Human Genetics","volume":"145 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149008414","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":"Polygenic risk scores in human genetics for study design discovery and translation.","authors":"Hui-Qi Qu, Hakon Hakonarson","doi":"10.1007/s00439-026-02873-y","DOIUrl":"10.1007/s00439-026-02873-y","url":null,"abstract":"<p><p>Polygenic risk scores (PRS) quantify the component of disease risk captured by measured additive common variants. Their use as a study design variable, rather than only as a predictive endpoint, broadens their scientific value in human genetics. PRS can define informative extremes of common-variant burden, identify discordance between phenotype and PRS-estimated risk, and facilitate the detection of subgroup-specific or residual mechanisms that may be obscured in conventional case-control analyses. This review outlines four major PRS-informed design strategies: tail sampling based on PRS extremes; discordance sampling based on mismatch between phenotype and PRS-implied risk; conditional and stratified genome-wide association analyses using PRS to adjust for / partition background risk; and residual phenotype analysis of the component of phenotype remaining after the PRS-associated component has been removed. It thus provides a practical framework for sample enrichment, subgroup definition, and calibrated epidemiologic comparison. These designs may be especially informative when integrated with sequencing, multi-omics, longitudinal cohorts, and translationally oriented intervention studies. Their application requires careful attention to data leakage, ancestry-related bias, collider structures, and the limits of interpretation.</p>","PeriodicalId":13175,"journal":{"name":"Human Genetics","volume":"145 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149008390","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":"Optical genome mapping improves structural variant detection and characterization in syndromic and neurogenetic disorders.","authors":"Rosa Catalina Lederbogen, Sabine Hoffjan, Cornelia Köhler, Charlotte Thiels, Ulrike Angelika Mau-Holzmann, Sylke Singer, Sabrina Schreiber, Anne Purczeld, Rebecca Buchert, Maria Viktorovna Yusenko, Hoa Huu Phuc Nguyen, Wanda Maria Gerding","doi":"10.1007/s00439-026-02856-z","DOIUrl":"10.1007/s00439-026-02856-z","url":null,"abstract":"<p><p>Optical Genome Mapping (OGM) offers superior resolution compared to standard diagnostic methods such as karyotyping and FISH, enabling the detection of nearly all types of chromosomal aberrations with non-centromeric breakpoints. This study evaluated OGM's potential to enhance the genetic findings in unsolved cases of neurogenetic and syndromic disease requiring further investigation after standard genetic testing. In 10 patients with various neurogenetic diagnoses, OGM confirmed all structural findings previously detected by karyotyping, chromosomal microarray (CMA), and/or NGS. Moreover, OGM provided additional structural insights in five cases, such as identifying a novel candidate gene in a patient with a balanced translocation, redefining of breakpoint regions in familial translocations, characterization of complex rearrangements, and revising of initial diagnostic interpretations. Most importantly, we present OGM results for three individuals with ring chromosomes 18, 20, and 22, highlighting the need to adjust filter settings and to incorporate the rare variant pipeline for accurate detection. Based on our experiences, we propose a strategic approach for identifying ring chromosomes using OGM. On the other hand, OGM did not identify causative variants in three unsolved cases with strong clinical suspicion of hereditary neuropathy. In summary, while OGM did not yield new insights for hereditary neuropathy, it provided additional or refined information in 6 out of 10 cases with other syndromic diseases. These findings underscore the value of OGM in increasing the diagnostic yield and precision of genetic testing.</p>","PeriodicalId":13175,"journal":{"name":"Human Genetics","volume":"145 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13562348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929660","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":"Development of RS1-specific ACMG/AMP variant classification criteria with pilot variant curation.","authors":"Sarah Hull, M Mero, W Hankey, K Lee, L S Sullivan, R Ayyagari, M D Benson, L Haer-Wigman, R B Hufnagel, H M J Hussain, K Kämpjärvi, P A Sieving, M Wang, G Wang, C Zeitz, R A Lewis, R Chen, K C Worley","doi":"10.1007/s00439-026-02871-0","DOIUrl":"10.1007/s00439-026-02871-0","url":null,"abstract":"<p><p>Gene-based therapies are being developed for retinal diseases, including RS1-related X-linked retinoschisis. Therefore it is essential to determine which variants are pathogenic and which are benign when enrolling patients. The Clinical Genome Resource (ClinGen) X-Linked Inherited Retinal Diseases (XLRD) Variant Curation Expert Panel (VCEP) brings together clinician scientists, molecular biologists, and geneticists to apply their expertise and review the clinical, genetic, population, and functional evidence for variants. American College of Medical Genetics (ACMG) guidelines have been modified for RS1 to develop a highly systematic and conservative framework for evaluating variants. The curation process involves applying 28 different codes, each with 4 strength levels (very strong, strong, moderate, supporting) across different domains of phenotype, population data, computational assessment, functional impact, and segregation. With RS1-specific rules, a total of 54 pilot variants were tested. These included 47 variants in ClinVar. Of these 21 variants were re-classified: 2 likely pathogenic variants and one likely benign were changed to variants of uncertain significance and 4 previously unclassified variants were changed to pathogenic, likely pathogenic and likely benign. Other changes resolved conflicts or multiple classifications.</p>","PeriodicalId":13175,"journal":{"name":"Human Genetics","volume":"145 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13545035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891440","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":"Integrating genetic, historical, and demographic evidence to reconstruct Argentina's matrilineal ancestry.","authors":"F Gagliardi, R Fernández, V Genoud, F Picado, S Biagini, N Furman, M Herrera Piñero, A C Mayordomo","doi":"10.1007/s00439-026-02870-1","DOIUrl":"10.1007/s00439-026-02870-1","url":null,"abstract":"<p><p>The Argentine population reflects a history of asymmetric admixture, a process particularly evident in uniparental markers. Consequently, the maternal lineage retains a record of the three primary ancestral origins: Native American, Eurasian, and African. The main objective of this study was to conduct an integrated comparative analysis to determine and assess the geographic distribution of mitochondrial haplogroups associated with these three ancestral origins across Argentina. This was achieved through an integrative approach that combined genetic data with census records and published literature. A dataset comprising 7,431 haplogroups analyzed at the provincial level was assembled from the literature. The overall maternal genetic composition obtained for the Argentine was 75% Native American, 22% Eurasian, and 3% African. However, significant regional and interprovincial heterogeneity were observed, which complicates broad genetic inferences. This work highlights the value of matrilineal markers in admixed societies for shedding light on population history and underscores the critical need to rigorously contextualize genetic results, given Argentina´s demographic and historical complexity.</p>","PeriodicalId":13175,"journal":{"name":"Human Genetics","volume":"145 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148860353","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":"From targeted SCN1A analysis to whole exome sequencing: clinical utility and novel genetic findings in a Hungarian paediatric epilepsy cohort.","authors":"Renata Szalai, Agnes Till, Krisztina Galimurka, Zsolt Banfai, Anna Zsigmond, Kinga Hadzsiev","doi":"10.1007/s00439-026-02867-w","DOIUrl":"10.1007/s00439-026-02867-w","url":null,"abstract":"<p><p>Epilepsy represents a highly prevalent neurological disorder with a significant genetic component, particularly implicating ion channel genes, including SCN1A. In this study, 431 individuals with heterogeneous paediatric-onset epilepsy phenotypes were assessed at the Department of Medical Genetics, University of Pécs between 2018 and 2024. Genetic investigations employed Sanger sequencing, targeted epilepsy gene panels, whole exome sequencing, and multiplex ligation-dependent probe amplification for SCN1A copy number analysis. Thirty-six pathogenic or likely pathogenic SCN1A variants were identified, including 15 variants which have not been reported previously. Furthermore, 9 novel variants were detected in 12 additional epilepsy-associated genes. Diagnostic yield was proportional to the breadth of genomic interrogation. WES analysis revealed 6 novel variants in 19 genes. These findings underscore the considerable genetic heterogeneity of epilepsy and demonstrate the clinical utility of gene panels and WES, particularly in complex phenotypes. The identification of novel variants enhances molecular understanding and facilitates more precise genotype-phenotype correlations, reinforcing the value of comprehensive genomic diagnostics in epilepsy management.</p>","PeriodicalId":13175,"journal":{"name":"Human Genetics","volume":"145 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13526097/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857317","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":"Expected costs and benefits of genetic counselling and germline genetic testing in metastatic prostate cancer.","authors":"Michiel Vlaming, Lambertus A L M Kiemeney, Wouter Koole, Inge M van Oort, Eveline M A Bleiker, Margreet G E M Ausems, Geert W J Frederix","doi":"10.1007/s00439-026-02854-1","DOIUrl":"10.1007/s00439-026-02854-1","url":null,"abstract":"<p><p>Identifying pathogenic germline variants in men with metastatic prostate cancer is important for therapeutic options and for identifying relatives who may have a high cancer risk. To keep genetic testing costs manageable, it is important to identify which patients should be selected for testing. In this study, we compared expected costs and number of identified pathogenic variants in two scenarios: offering genetic testing to all men with metastatic prostate cancer versus testing only those with additional risk factors linked to a higher likelihood of carrying a pathogenic variant. Costs were evaluated with a mainstream genetic testing pathway, where testing is discussed by a non-genetic healthcare professional. Using Dutch national incidence data, predefined healthcare cost frameworks, and a hypothetical assumption for the acceptance rate of patients, we modelled total costs for the Netherlands and number of identified pathogenic variants for each approach. The costs of genetic testing and post-test counselling decreased threefold when applying selection criteria, compared to the scenario where all metastatic prostate cancer patients are eligible. However, applying selection criteria would result in missing 41% clinically relevant pathogenic germline variants that would otherwise be identified. This implies that, at national level, a discussion should be started regarding willingness to pay for identifying pathogenic germline variants.</p>","PeriodicalId":13175,"journal":{"name":"Human Genetics","volume":"145 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13526062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857266","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":"Genomic characterization of historical Jinlingnan individuals: insights into genetic continuity and trans-Eurasian signals in eastern China.","authors":"Shuyi Li, Yuchun Wang, Qu Shen, Jinguo Zan, Mengying Han, Zishuai Huang, Rui Wang, Xinyi Wang, Haifeng He, Le Tao, Hao Ma, Kongyang Zhu, Yetao Zou, Huangzhen Huang, Haodong Chen, Li Jin, Hui Li, Chuan-Chao Wang","doi":"10.1007/s00439-026-02864-z","DOIUrl":"10.1007/s00439-026-02864-z","url":null,"abstract":"<p><p>The genetic impact of historically documented trans-Eurasian interactions in China remains poorly understood due to the scarcity of genome-wide ancient DNA data. This study presents genome-wide SNP data from 10 individuals excavated from the Jinlingnan cemetery in Zibo City, Shandong Province, dating from the Tang (618-907 AD) to the Qing (1644-1912 AD) dynasties. Although located in the agricultural heartland of eastern China rather than along major Silk Road corridors, the site provides a valuable context for investigating the integration of non-local populations into inland societies. Our analyses reveal that the Jinlingnan individuals primarily derived their ancestry from the Middle Yellow River region, showing strong genetic continuity with both contemporaneous and modern northern Chinese populations. Notably, a subset of seven individuals exhibited detectable genetic contributions from Western Eurasians or Central Asians, with proportions ranging from 1.5% to 12.1%, providing direct evidence of gene flow from trans-Eurasian interactions. Furthermore, modern Han populations in Shandong can be modeled as deriving the vast majority of their ancestry (~ 95%) from a Jinlingnan-related source, with a minor contribution (~ 5%) from southern Chinese-related groups. These results delineate the demographic history of the Jinlingnan population, characterized by foundational Central Plains continuity, localized incorporation of exogenous components, and subsequent north-south interactions. This study demonstrates that the demographic impact of trans-Eurasian exchange extended far beyond Silk Road hubs, reaching deep into inland eastern China.</p>","PeriodicalId":13175,"journal":{"name":"Human Genetics","volume":"145 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818258","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":"Clinical and zebrafish studies of truncating SF3B2-variants in craniofacial microsomia.","authors":"Dan Xia, Xiaofang Peng, Zihao Deng, Shuyun Deng, Zhanwen He, Jieming Zhang, Xiaoqin Xiao, Xi Sun, Xiao Qian, Xueyuan Zhang, Liyang Liang, Xiaojuan Li","doi":"10.1007/s00439-026-02860-3","DOIUrl":"10.1007/s00439-026-02860-3","url":null,"abstract":"<p><p>Craniofacial microsomia (CFM) exhibits significant phenotypic variability and degree of severity. While loss-of-function variants in SF3B2 have recently emerged as a genetic etiology, the molecular basis underlying this clinical heterogeneity remains poorly understood. Here, we report two probands harboring novel truncating SF3B2 variants and presenting with distinct clinical phenotypes. Proband 1, with a heterozygous p.(Gln60*) variant, exhibited characteristic CFM features, including mandibular hypoplasia, cleft palate, bilateral tragal abnormalities, microtia, external auditory canal stenosis with hearing impairment, and an epibulbar dermoid. In contrast, Proband 2, carrying a p.(Lys507*) variant, exhibited a milder craniofacial phenotype, although he had hearing loss and developmental delay that could not be explained with certainty by the SF3B2-variant. Western blot analysis demonstrated complete loss of p.(Gln60*) protein, whereas the p.(Lys507*) variant-despite lying outside the predicted nonsense-mediated decay (NMD) escape region-retained 15.5% residual expression of truncated protein. To investigate functional consequences, we performed CRISPR/Cas9-mediated sf3b2 knockout in zebrafish. Mutant larvae showed a 25.33% malformation rate and recapitulated human craniofacial features, including a reduced head-to-body length ratio (p = 0.0013), hypoplastic mandibular cartilage-evidenced by shortened Meckel's cartilage (p = 0.0104) and Palatoquadrate (p = 0.0174)-and impaired skeletal mineralization (p = 0.0028). Together, these findings suggest that truncating variants at different positions may be associated with differential protein expression levels and variable clinical presentations. Our study reinforces SF3B2's role as a loss-of-function disease gene and highlights the importance of variant-specific molecular characterization in understanding CFM.</p>","PeriodicalId":13175,"journal":{"name":"Human Genetics","volume":"145 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792519","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}