Nature genetics最新文献

{"title":"Multi-ancestry genome-wide association study of severe pregnancy nausea and vomiting","authors":"Marlena Fejzo, Xinran Wang, Qing Tan, Julia Zöllner, Natàlia Pujol-Gualdo, Triin Laisk, Estonian Biobank Research Team, Sarah Finer, David A. van Heel, Health Research Team, Ben Brumpton, Laxmi Bhatta, Kristian Hveem, Elizabeth A. Jasper, Digna R. Velez Edwards, Jacklyn N. Hellwege, Todd Edwards, Gail P. Jarvik, Yuan Luo, Atlas Khan, Kimber MacGibbon, Yuan Gao, Gaoxiang Ge, Inna Averbukh, Erin Soon, Michael Angelo, Per Magnus, Stefan Johansson, Pål R. Njølstad, Artem Kim, Steven Gazal, Marc Vaudel, Chang April Shu, Nicholas Mancuso","doi":"10.1038/s41588-026-02564-4","DOIUrl":"10.1038/s41588-026-02564-4","url":null,"abstract":"Most pregnancies are affected by nausea and vomiting, but the most severe form—hyperemesis gravidarum—can be life threatening. Here we performed a multi-ancestry genome-wide association study of hyperemesis gravidarum in 10,974 cases and 461,461 controls across European, Asian, African and Latino ancestries. We identified ten associations: four identified previously (GDF15, IGFBP7, PGR and GFRAL) and six additional loci (SLITRK1, SYN3, IGSF11, FSHB, TCF7L2 and CDH9). Downstream analyses revealed GDF15 and TCF7L2 expression primarily in extravillous trophoblasts, with opposing effects for GDF15 between maternal and fetal genotype. Conversely, IGFBP7 and PGR were expressed primarily in maternal spiral arteries, with effects limited to the maternal genome. Selected loci were associated with abnormal pregnancy weight gain, duration, birth weight and pre-eclampsia. Functional studies identified additional associations including antisense IGFBP7-AS1 and protein ACP1. Potential roles for candidate genes in appetite, insulin signaling and brain plasticity provide pathways to explore etiological mechanisms and therapeutic avenues. Multi-ancestry GWAS meta-analysis identifies risk loci for severe nausea and vomiting of pregnancy. Downstream analyses explore maternal and fetal contributions of these loci and their temporal effects.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"58 4","pages":"810-820"},"PeriodicalIF":29.0,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147680368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Postmitotic transcription and 3D regulation show locus-specific and differentiation-specific sensitivity to cohesin depletion","authors":"UkJin Lee, Alejandra Laguillo-Diego, Daniela Magliulo, Wilfred Wong, Kritika Kasliwal, Zhangli Ni, Lingling Cheng, Jieru Li, Bobbie Pelham-Webb, Alexandros Pertsinidis, Christina Leslie, Effie Apostolou","doi":"10.1038/s41588-026-02556-4","DOIUrl":"10.1038/s41588-026-02556-4","url":null,"abstract":"Acute cohesin loss causes widespread reorganization of three-dimensional (3D) chromatin architecture but has relatively minor effects on steady-state transcription. It remains unclear whether its role in gene regulation becomes more critical during mitotic exit, when 3D chromatin architecture and transcription are globally re-established. To address this, we acutely depleted RAD21 in mouse embryonic stem cells during mitotic exit under self-renewal or differentiation conditions. Here we show that, although most loops failed to reform without cohesin, the few cohesin-independent loops were linked to active promoters, strong enhancers and H3K27ac mitotic bookmarking. Transcriptional changes were only modest, indicating that gene reactivation largely bypasses cohesin. Sensitive genes showed RAD21 promoter binding, a higher number of structural loops and positioning within well-insulated, gene-poor topologically associating domains. During differentiation, cohesin loss impaired activation of a broader set of developmental genes, partly due to defective de novo regulatory interactions. Together, these findings demonstrate context-specific requirements for cohesin in gene activation. Lee et al. deplete the cohesin component RAD21 in mouse embryonic stem cells. Most but not all chromatin loops fail to reform after mitosis, and transcriptional changes were minor, except during differentiation, where cohesin seems to have a more important role.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"58 4","pages":"892-902"},"PeriodicalIF":29.0,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147666552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"De novo formation of cis-regulatory contacts in the absence of NIPBL-driven chromatin loop extrusion","authors":"Nicholas G. Aboreden, Han Zhao, Jin H. Yang, Fengnian Shan, Fuhai Liu, Anders S. Hansen, Haoyue Zhang, Gerd A. Blobel","doi":"10.1038/s41588-026-02565-3","DOIUrl":"10.1038/s41588-026-02565-3","url":null,"abstract":"NIPBL promotes chromatin loop extrusion by the cohesin complex until it stalls at convergently oriented CTCF sites, forming structural loops. While a large fraction of loops connecting cis-regulatory elements (CREs) can be maintained in cohesin-depleted cells, whether the loop extrusion process contributes to the de novo establishment of CRE loops remains unclear. To address this question, we characterized the formation of structural and CRE loops in NIPBL-depleted cells during the mitosis-to-G1-phase transition. Structural loop formation was impaired proportionally to loop length. Computational modeling supports these observations, suggesting that NIPBL promotes both cohesin loading and extrusion. Notably, most CRE loops, regardless of length, were established normally upon NIPBL degradation. While a subset of contacts among weak CREs were formed with delayed kinetics in NIPBL-depleted cells, generally gene activation was only mildly impaired. Collectively, our findings suggest that postmitotic establishment of regulatory contacts and gene transcription can occur independently of chromatin loop extrusion. The authors deplete the cohesin activator NIPBL during the mitosis-to-G1-phase transition. They observe that structural loop formation is impaired proportionally to loop length, while gene activation and enhancer–promoter interactions are only mildly impaired.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"58 4","pages":"881-891"},"PeriodicalIF":29.0,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147666553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone acetylation-dependent clustering of BRD2 instructs transcription dynamics","authors":"Niyazi Umut Erdogdu, Sukanya Guhathakurta, Ronald Oellers, Maria Shvedunova, Jose A. Morin, Eric M. Patrick, Janine Seyfferth, Ward Deboutte, Alejandro Gomez-Auli, Gerhard Mittler, Ibrahim I. Cissé, Asifa Akhtar","doi":"10.1038/s41588-026-02533-x","DOIUrl":"10.1038/s41588-026-02533-x","url":null,"abstract":"Bromodomain (BD) and extra-terminal domain (BET) proteins are key regulators of RNA polymerase II (Pol II)-mediated transcription and their BDs represent promising drug targets. Yet, the interplay between histone acetylation and the chromatin dynamics of individual BET proteins with respect to transcriptional regulation is not fully understood. Here in mouse embryonic stem cells, we uncover an essential role of BRD2 in maintaining Pol II recruitment at promoters through its interaction with TFIID, which becomes particularly critical under the conditions of impaired pause release. Combining rapid protein degradation, chemogenomics and super-resolution microscopy, we show that MOF-mediated histone H4 acetylation promotes BRD2 chromatin association, which in turn enables BRD2 clustering. Accordingly, MOF depletion or deletion of the BRD2’s intrinsically disordered region largely recapitulates defects in promoter enrichment and clustering of the transcription machinery observed upon BRD2 loss. Thus, these findings support a model in which histone acetylation-dependent spatiotemporal dynamics of BRD2 coordinate the transcription machinery to regulate transcription initiation. BRD2 is key for RNA polymerase II recruitment at promoters, becoming critical in the absence of BRD4 or upon pause-release inhibition. Depletion of MOF or deletion of BRD2’s intrinsically disordered region mimics transcriptional defects caused by BRD2 loss.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"58 4","pages":"854-868"},"PeriodicalIF":29.0,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-026-02533-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147641443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-content genetic screens identify RNA-based mechanisms to target immune evasion","authors":"","doi":"10.1038/s41588-026-02563-5","DOIUrl":"10.1038/s41588-026-02563-5","url":null,"abstract":"With a focus on RNA-based interventions, we identify a suite of previously underappreciated and functionally diverse genes that control cancer cell susceptibility to targeted T cell-mediated elimination. We further introduce a scalable strategy to decode the functions of these regulators by combining gain-of-function screening with single-cell and optical high-content genetic approaches.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"58 4","pages":"685-686"},"PeriodicalIF":29.0,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147641750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biallelic variants in the noncoding RNA gene RNU4-2 cause a recessive neurodevelopmental syndrome with distinct white matter changes","authors":"Rocio Rius, Alexander J. M. Blakes, Yuyang Chen, Joachim De Jonghe, François Lecoquierre, Ruebena Dawes, Benjamin Cogne, Hyung Chul Kim, Javeria R. Alvi, Florence Amblard, Morad Ansari, Annabelle Arlt, Christina Austin-Tse, Sarah Baer, Meena Balasubramanian, Elsa V. Balton, Giulia Barcia, Ana Beleza-Meireles, Jonathan A. Bernstein, Jasmin Beygo, Pierre Blanc, Nuria C. Bramswig, Frederik Braun, Daniel Buchzik, Daniel G. Calame, Jamie Campbell, Charles Coutton, Chloe A. Cunningham, Nitsuh Dargie, Christel Depienne, Katrina M. Dipple, Anne Dieux, Abhijit Dixit, Lauren Dreyer, Haowei Du, Salima El Chehadeh, Michael Field, Lisa J. Ewans, Vanessa Geiger, Richard A. Gibbs, Ian Glass, Olivier Grunewald, Paul Gueguen, Tobias B. Haack, Hamza Hadj Abdallah, Radu Harbuz, Ingo Helbig, Judit Horvath, Alexander Hustinx, Bertrand Isidor, Marie-Line Jacquemont, Fraser Jamie, Médéric Jeanne, Riley Kessler, Hannah Klinkhammer, G. Christoph Korenke, Urania Kotzaeridou, Peter Krawitz, Steven Laurie, Richard J. Leventer, Rebecca J. Levy, James R. Lupski, Pierre Marijon, Kaitlin E. McGinnis, Rodrigo Mendez, Olfa Messaoud, Caroline Nava, Mevyn Nizard, Anne O’Donnell-Luria, Melanie C. O’Leary, Simone Olivieri, Amitav Parida, Davut Pehlivan, Anna Jenne Prentice, Jennifer E. Posey, Chloe M. Reuter, Véronique Satre, Caroline Schluth-Bolard, Thomas Smol, Tipu Sultan, John Taylor, Christel Thauvin-Robinetvin, Julien Thevenon, Eloise Uebergang, Sandra Ueberberg, Catherine Vincent-Delorme, Evangeline Wassmer, Emma Westwood, Matthew T. Wheeler, Elif Yilmaz Gulec, Adeline Vanderver, Arastoo Vossough, Stephan J. Sanders, Siddharth Banka, Gregory M. Findlay, Daniel G. MacArthur, Cas Simons, Nicola Whiffin","doi":"10.1038/s41588-026-02554-6","DOIUrl":"10.1038/s41588-026-02554-6","url":null,"abstract":"Genetic variants in RNU4-2, which is transcribed into the U4 small nuclear RNA component of the major spliceosome, were recently shown to cause ReNU syndrome, a prevalent dominant neurodevelopmental disorder (NDD). These variants almost exclusively arise de novo and cluster within 18 nucleotides of RNU4-2. Here we describe a new recessive NDD associated with homozygous and compound heterozygous variants in RNU4-2. We identify 38 individuals with biallelic variants outside the 18-nucleotide ReNU syndrome region that cluster within other functionally important elements of U4: Stem II, the k-turn and the Sm protein binding site. We characterize the clinical phenotype in 31 individuals, demonstrating that the recessive disorder is clinically distinct from ReNU syndrome and is associated with distinctive white matter abnormalities, including enlarged perivascular spaces. Finally, we find reduced RNU4-2 transcript levels in individuals with the recessive disorder, suggesting a loss-of-function disease mechanism that is distinct from the mechanism underlying ReNU syndrome. Together, these findings expand the genotypic and phenotypic spectrum of RNU4-2-associated NDDs. Biallelic variants in RNU4-2 cause a recessive neurodevelopmental disorder that is phenotypically and molecularly distinct from dominant ReNU syndrome and associated with reduced RNU4-2 transcript levels, consistent with a loss-of-function mechanism.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"58 4","pages":"761-773"},"PeriodicalIF":29.0,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-026-02554-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147631136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Publisher Correction: A meta-analysis of single-nucleus expression quantitative trait loci linking genetic risk to brain disorders","authors":"Beomjin Jang, Kailash BP, Alex Tokolyi, Winston H. Dredge, Ashvin Ravi, Sang-Hyuk Jung, Tatsuhiko Naito, Beomsu Kim, Min Seo Kim, Minyoung Cho, Mi-So Park, Mikaela Rosen, Joel Blanchard, Jack Humphrey, David A. Knowles, Hong-Hee Won, Towfique Raj","doi":"10.1038/s41588-026-02581-3","DOIUrl":"10.1038/s41588-026-02581-3","url":null,"abstract":"","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"58 4","pages":"953-953"},"PeriodicalIF":29.0,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-026-02581-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147633876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-content CRISPR activation screens identify synthetically lethal RNA-based mechanisms to sensitize cancer cells to targeted T cell cytotoxicity","authors":"Reece Villarin Akana, Jeehyun Yoe, Olivia Laveroni, Chang Sun, Young-Min Kim, Livnat Jerby","doi":"10.1038/s41588-026-02561-7","DOIUrl":"10.1038/s41588-026-02561-7","url":null,"abstract":"T cells recognize their target cells through the T cell receptor (TCR). Combining gain-of-function, single-cell and optical high-content screens, we identified RNA-based mechanisms that selectively sensitize target cells to TCR-specific T cell cytotoxicity. First, CRISPR activation screens in melanoma cells identify functionally diverse regulators of TCR-specific cytotoxicity, including SAFB, KHDRBS1, MYC, CD44, WNT3A, WNT1 and others. Expressing sensitizing hits in cancer and virally infected cells restores TCR-specific cytotoxicity. Next, we developed in situ Perturb-seq for optical pooled genetic screens with in situ detection of perturbations and spatial transcriptomic readouts. Perturb-seq and in vivo–in situ Perturb-seq show that the hits converge on shared cell-autonomous and intercellular mechanisms, map gene–environment interactions and reveal that Wnt ligands activate T cells. Introducing a scalable approach to decode gene function at the cell and tissue level, the study uncovered context-specific gene functions to restore targeted T cell-based elimination of dysfunctional cells via synthetically lethal, RNA-based interventions. A series of in vitro and in vivo CRISPR activation screens combined with in situ Perturb-seq identify regulators of T cell-dependent cytotoxicity in melanoma.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"58 4","pages":"841-853"},"PeriodicalIF":29.0,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-026-02561-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147630288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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 potential of wheat spatial omics.","authors":"Xiao-Yuan Tao,Cong Tan,Yifan Liu,Yuanyuan Wang,Ali Raza,Jing He,Lulu Wang,Keke Xia,Yan Yan,Sha Liao,Wei Jiang,Yue Qu,Bo Xu,Yi Zhou,Xiujuan Yang,Stuart Roy,Matthew Denton,Matthew Tucker,Jason Able,Matthew Gilliham,Peter Langridge,Hang-Wei Hu,Ji-Zheng He,Chenchen Zhao,Meixue Zhou,Reyazul Rouf Mir,Annapurna Chitikineni,Chengdao Li,Peng Zhang,Richard Trethowan,Yi Ding,Jianping Zhang,Peter Franks,Qiuhong Wu,Lingzhen Ye,Yizhou Wang,Feibo Wu,Guoping Zhang,Shengguan Cai,Qiufang Shen,Hangjin Jiang,Guang Chen,Yun Zhou,Chunpeng Song,Yumei Zhang,Wujun Ma,Ximei Li,Weiwei Guo,Jianbin Zeng,Xiaoyan He,Wenxing Liu,Xue Feng,Rongzhi Zhang,Genying Li,Xinyou Cao,Shubing Liu,Qier Liu,Jiansheng Chen,Xueyong Zhang,Luxiang Liu,Fanrong Zeng,Fenglin Deng,Yuan Qin,Xiangqian Zhu,Sergey Shabala,Estee E Tee,Thorsten Schnurbusch,Martin Mascher,Honghong Wu,Manuel Spannagl,Mingming Xin,Jinying Gou,Gurcharn Brar,Dawei Xue,Wei Wang,Matthew Reynolds,Yusheng Zhao,Zhiyong Liu,Tamar Krugman,Yoichi Sakata,Suyan Yee,Kai Chan,Barry Pogson,Yijing Zhang,D Blaine Marchant,Kadambot H M Siddique,Xiaodong Fang,Ao Chen,Robert Henry,Scott A Boden,Rajeev K Varshney,Sheng-Chun Xu,Xun Xu,Zhong-Hua Chen","doi":"10.1038/s41588-026-02542-w","DOIUrl":"https://doi.org/10.1038/s41588-026-02542-w","url":null,"abstract":"Wheat is a major staple crop for over one-third of the world's population, crucial for global food security, economic stability and cultural traditions. Recently, single-cell and spatial omics approaches have transformed biological discovery, primarily in medical and animal sciences, and they are now beginning to be applied in plant research. Here we summarize the technical innovations and feasibility of spatial omics applications in wheat research, particularly for understanding developmental and environmental responses, thereby potentially enhancing wheat breeding. We highlight how these tools can reveal spatial and temporal patterns in gene expression, cellular heterogeneity and tissue organization in wheat. Furthermore, we propose developing a spatially resolved single-cell atlas of wheat across its life cycle to facilitate breakthroughs in basic research and potential applications in breeding. To achieve these goals, we advocate for a Wheat Spatial Omics Consortium to foster worldwide collaboration for overcoming barriers and developing sustainable and climate-resilient wheat.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"64 1","pages":""},"PeriodicalIF":30.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147585752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heterogeneity of leukocyte telomere length and its associations with phenotypes and genotypes","authors":"","doi":"10.1038/s41588-026-02566-2","DOIUrl":"10.1038/s41588-026-02566-2","url":null,"abstract":"Leukocyte telomere length (LTL) has been associated with various health-related traits, with heterogeneity across specific demographic factors. Rich phenotypic and genomic data collected by the National Institutes of Health (NIH) All of Us Research Program from diverse US populations provided the opportunity to systematically assess the heterogeneity of the genomic, phenomic and geographic associations of LTL.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"58 4","pages":"683-684"},"PeriodicalIF":29.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147585409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}