{"title":"Closing 2025, and a look ahead","authors":"","doi":"10.1038/s41594-025-01732-0","DOIUrl":"10.1038/s41594-025-01732-0","url":null,"abstract":"We review 2025 and discuss some of the foremost initiatives developed at the journal. We also look back at discoveries we have been proud to publish.","PeriodicalId":49141,"journal":{"name":"Nature Structural & Molecular Biology","volume":"32 12","pages":"2373-2373"},"PeriodicalIF":10.1,"publicationDate":"2025-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41594-025-01732-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145730583","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}
Pub Date : 2025-12-10DOI: 10.1038/s41594-025-01725-z
Ifigenia Tsitsa, Anja Conev, Alessia David, Suhail A. Islam, Michael J. E. Sternberg
The AlphaFold database, released in 2022, modeled UniProt sequences from April 2021 and now provides 200 million predicted protein structures. Of the 20,504 full-length predicted human structures, 631 entries conflict with the June 2025 UniProt release. Similar conflicts across species highlight how bioinformatics resources can rapidly age.
{"title":"The aging of the AlphaFold database","authors":"Ifigenia Tsitsa, Anja Conev, Alessia David, Suhail A. Islam, Michael J. E. Sternberg","doi":"10.1038/s41594-025-01725-z","DOIUrl":"10.1038/s41594-025-01725-z","url":null,"abstract":"The AlphaFold database, released in 2022, modeled UniProt sequences from April 2021 and now provides 200 million predicted protein structures. Of the 20,504 full-length predicted human structures, 631 entries conflict with the June 2025 UniProt release. Similar conflicts across species highlight how bioinformatics resources can rapidly age.","PeriodicalId":49141,"journal":{"name":"Nature Structural & Molecular Biology","volume":"32 12","pages":"2374-2376"},"PeriodicalIF":10.1,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145717909","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}
Pub Date : 2025-12-07DOI: 10.1038/s41594-025-01734-y
Taylor L. Mighell, Ben Lehner
{"title":"Author Correction: A small molecule stabilizer rescues the surface expression of nearly all missense variants in a GPCR","authors":"Taylor L. Mighell, Ben Lehner","doi":"10.1038/s41594-025-01734-y","DOIUrl":"10.1038/s41594-025-01734-y","url":null,"abstract":"","PeriodicalId":49141,"journal":{"name":"Nature Structural & Molecular Biology","volume":"32 12","pages":"2633-2633"},"PeriodicalIF":10.1,"publicationDate":"2025-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41594-025-01734-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145701269","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}
Pub Date : 2025-12-03DOI: 10.1038/s41594-025-01724-0
Elizabeth T. Abshire, Lynne E. Maquat
The exon junction complex (EJC) begins to assemble on the spliceosome, which deposits EJCs upstream of most exon–exon junctions during pre-messenger RNA (mRNA) splicing. EJCs acquire additional alternative modules that define heterogeneous EJCs during pre-mRNA processing to mRNA in the nucleus and after mRNA export into the cytoplasm. In this Review, we discuss the mechanisms of EJC formation, the many roles of the EJC in pre-mRNA and mRNA regulation and how these roles are influenced by EJC composition. This Review summarizes the various functions of the exon junction complex in RNA splicing and beyond, to influence gene regulation.
{"title":"Gene regulation through exon junction complex modularity","authors":"Elizabeth T. Abshire, Lynne E. Maquat","doi":"10.1038/s41594-025-01724-0","DOIUrl":"10.1038/s41594-025-01724-0","url":null,"abstract":"The exon junction complex (EJC) begins to assemble on the spliceosome, which deposits EJCs upstream of most exon–exon junctions during pre-messenger RNA (mRNA) splicing. EJCs acquire additional alternative modules that define heterogeneous EJCs during pre-mRNA processing to mRNA in the nucleus and after mRNA export into the cytoplasm. In this Review, we discuss the mechanisms of EJC formation, the many roles of the EJC in pre-mRNA and mRNA regulation and how these roles are influenced by EJC composition. This Review summarizes the various functions of the exon junction complex in RNA splicing and beyond, to influence gene regulation.","PeriodicalId":49141,"journal":{"name":"Nature Structural & Molecular Biology","volume":"32 12","pages":"2387-2397"},"PeriodicalIF":10.1,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145664342","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}
Pub Date : 2025-12-03DOI: 10.1038/s41594-025-01730-2
Ok-Ho Shin, Jun Lu, Jeong-Seop Rhee, Diana R. Tomchick, Zhiping P. Pang, Sonja M. Wojcik, Marcial Camacho-Perez, Nils Brose, Mischa Machius, Josep Rizo, Christian Rosenmund, Thomas C. Südhof
{"title":"Editorial Expression of Concern: Munc13 C2B domain is an activity-dependent Ca2+ regulator of synaptic exocytosis","authors":"Ok-Ho Shin, Jun Lu, Jeong-Seop Rhee, Diana R. Tomchick, Zhiping P. Pang, Sonja M. Wojcik, Marcial Camacho-Perez, Nils Brose, Mischa Machius, Josep Rizo, Christian Rosenmund, Thomas C. Südhof","doi":"10.1038/s41594-025-01730-2","DOIUrl":"10.1038/s41594-025-01730-2","url":null,"abstract":"","PeriodicalId":49141,"journal":{"name":"Nature Structural & Molecular Biology","volume":"32 12","pages":"2634-2634"},"PeriodicalIF":10.1,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41594-025-01730-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145664012","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}
Pub Date : 2025-11-27DOI: 10.1038/s41594-025-01720-4
Cells store excess fat in lipid droplets to avoid lipotoxicity and maintain homeostasis. We identified an autophagy-independent role for the autophagy lipid transfer protein ATG2A in helping direct lipids to growing lipid droplets and promoting recruitment of the enzyme DGAT2. This coordination enhances triglyceride storage, protects the endoplasmic reticulum from lipid overload and limits the misrouting of lipids into other metabolic pathways.
{"title":"ATG2A–DGAT2 cooperation fuels lipid droplet growth","authors":"","doi":"10.1038/s41594-025-01720-4","DOIUrl":"10.1038/s41594-025-01720-4","url":null,"abstract":"Cells store excess fat in lipid droplets to avoid lipotoxicity and maintain homeostasis. We identified an autophagy-independent role for the autophagy lipid transfer protein ATG2A in helping direct lipids to growing lipid droplets and promoting recruitment of the enzyme DGAT2. This coordination enhances triglyceride storage, protects the endoplasmic reticulum from lipid overload and limits the misrouting of lipids into other metabolic pathways.","PeriodicalId":49141,"journal":{"name":"Nature Structural & Molecular Biology","volume":"32 12","pages":"2385-2386"},"PeriodicalIF":10.1,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145609471","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}
Pub Date : 2025-11-20DOI: 10.1038/s41594-025-01722-2
Heesoo Uhm, Sangsu Bae
Artificial intelligence (AI) is advancing genome editing, from predictive modeling to generative design. Emerging generative AI tools such as RFdiffusion, AlphaFold 3 and ESM now facilitate the de novo design of linkers, inhibitors and enzymes. We highlight work where AI-driven design is used to enhance the precision of mitochondrial cytosine base editors.
{"title":"Expansion of artificial intelligence for genome editing","authors":"Heesoo Uhm, Sangsu Bae","doi":"10.1038/s41594-025-01722-2","DOIUrl":"10.1038/s41594-025-01722-2","url":null,"abstract":"Artificial intelligence (AI) is advancing genome editing, from predictive modeling to generative design. Emerging generative AI tools such as RFdiffusion, AlphaFold 3 and ESM now facilitate the de novo design of linkers, inhibitors and enzymes. We highlight work where AI-driven design is used to enhance the precision of mitochondrial cytosine base editors.","PeriodicalId":49141,"journal":{"name":"Nature Structural & Molecular Biology","volume":"32 12","pages":"2380-2382"},"PeriodicalIF":10.1,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145554401","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}
Pub Date : 2025-11-17DOI: 10.1038/s41594-025-01715-1
Domagoj Baretić, Sophia Missoury, Karishma Patel, Maximilien Martinez, Franck Coste, Kang Zhu, Rebecca Smith, Anna Georgina Kopasz, Yang Lu, Nicolas Bigot, Catherine Chapuis, Romane Riou, Nina Đukić, Stéphane Goffinont, Valentin Pressoir, Sara Patačko, Gyula Timinszky, Marc Delarue, Bertrand Castaing, Dragana Ahel, Andreja Mikoč, Sébastien Huet, Ivan Ahel, Marcin J. Suskiewicz
Sirtuins are an ancient family of enzymes with diverse nicotinamide adenine dinucleotide (NAD)-dependent activities. Here we identify family with sequence similarity 118 member B (FAM118B) and FAM118A—two understudied vertebrate proteins—as vertebrate-specific sirtuins with similarities to bacterial antiphage sirtuins. We show that human FAM118B forms head-to-tail filaments both in vitro and in living human cells, a feature that appears to be conserved in both FAM118B and its paralog FAM118A across vertebrates. While human FAM118B and FAM118A have individually very weak NAD-processing activity in vitro, their interaction leads to markedly increased activity, suggesting a tightly regulated system. The overexpression of wild-type human FAM118B and FAM118A leads to strongly decreased NAD levels in human cells, an effect that is abolished in catalytically dead or filament-deficient mutants. Our study highlights filament formation and NAD processing as conserved mechanisms among immunity-associated sirtuins across evolution. Baretić and Missoury et al. identify vertebrate proteins FAM118B and FAM118A as sirtuins similar to bacterial antiphage enzymes and show that FAM118A/B processing of NAD involves head-to-tail filament formation and a partnership between the two paralogs.
{"title":"Filament formation and NAD processing by noncanonical human FAM118 sirtuins","authors":"Domagoj Baretić, Sophia Missoury, Karishma Patel, Maximilien Martinez, Franck Coste, Kang Zhu, Rebecca Smith, Anna Georgina Kopasz, Yang Lu, Nicolas Bigot, Catherine Chapuis, Romane Riou, Nina Đukić, Stéphane Goffinont, Valentin Pressoir, Sara Patačko, Gyula Timinszky, Marc Delarue, Bertrand Castaing, Dragana Ahel, Andreja Mikoč, Sébastien Huet, Ivan Ahel, Marcin J. Suskiewicz","doi":"10.1038/s41594-025-01715-1","DOIUrl":"10.1038/s41594-025-01715-1","url":null,"abstract":"Sirtuins are an ancient family of enzymes with diverse nicotinamide adenine dinucleotide (NAD)-dependent activities. Here we identify family with sequence similarity 118 member B (FAM118B) and FAM118A—two understudied vertebrate proteins—as vertebrate-specific sirtuins with similarities to bacterial antiphage sirtuins. We show that human FAM118B forms head-to-tail filaments both in vitro and in living human cells, a feature that appears to be conserved in both FAM118B and its paralog FAM118A across vertebrates. While human FAM118B and FAM118A have individually very weak NAD-processing activity in vitro, their interaction leads to markedly increased activity, suggesting a tightly regulated system. The overexpression of wild-type human FAM118B and FAM118A leads to strongly decreased NAD levels in human cells, an effect that is abolished in catalytically dead or filament-deficient mutants. Our study highlights filament formation and NAD processing as conserved mechanisms among immunity-associated sirtuins across evolution. Baretić and Missoury et al. identify vertebrate proteins FAM118B and FAM118A as sirtuins similar to bacterial antiphage enzymes and show that FAM118A/B processing of NAD involves head-to-tail filament formation and a partnership between the two paralogs.","PeriodicalId":49141,"journal":{"name":"Nature Structural & Molecular Biology","volume":"32 12","pages":"2526-2541"},"PeriodicalIF":10.1,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41594-025-01715-1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145531502","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}
Pub Date : 2025-11-17DOI: 10.1038/s41594-025-01689-0
Helin Elhan, Alicia Damm, Justin L. Korfhage, Daniel Álvarez, Mehdi Zouiouich, Francesca Giordano, Stefano Vanni, Thomas J. Melia, Abdou Rachid Thiam
Lipid droplet (LD) growth mechanisms and the roles of LD-associated lipid transfer proteins remain poorly understood. Here we show that the autophagy lipid transfer protein ATG2A has an anabolic role and promotes LD expansion by transferring diacylglycerol (DAG), triacylglycerol (TAG) and phosphatidic acid, from the endoplasmic reticulum to LDs. In ATG2A deficiency, synthesized lipids are incorporated inefficiently into LDs and assemble new LDs. In addition, DAG O-acyltransferase 2 (DGAT2), which synthesizes TAG and expands LD, fails to relocate to LDs. In vitro, DAG recruits DGAT2 to LDs. These findings support the idea that ATG2A-mediated DAG transfer recruits DGAT2 to LDs, promoting LD expansion. ATG2A alone promotes LD growth by transferring TAG and DAG, but its effectiveness in LD expansion is reduced when DGAT2 is inhibited. This synergistic action with DGAT2 prevents the buildup of nonmembrane lipids within the endoplasmic reticulum and favors TAG synthesis on the LD surface. Elhan et al. show that ATG2A acts with DGAT2, the enzyme producing triacylglycerol (TAG), in lipid droplet growth. By delivering diacylglycerol to lipid droplets, ATG2A not only fuels TAG production but also promotes the recruitment of DGAT2 to droplet surfaces.
脂滴（LD）的生长机制和LD相关的脂质转移蛋白的作用仍然知之甚少。本研究表明，自噬脂质转移蛋白ATG2A具有合成代谢作用，通过将二酰基甘油（DAG）、三酰基甘油（TAG）和磷脂酸从内质网转移到LD，促进LD扩张。在ATG2A缺乏的情况下，合成的脂质不能有效地结合到ld中并组装新的ld。此外，合成TAG并扩展LD的DAG o -酰基转移酶2 （DGAT2）无法迁移到LD上。在体外，DAG将DGAT2招募到ld。这些发现支持了atg2a介导的DAG转移将DGAT2招募到LD，促进LD扩展的观点。单独ATG2A通过转移TAG和DAG促进LD生长，但当DGAT2被抑制时，其对LD扩展的作用降低。这种与DGAT2的协同作用可防止内质网内非膜脂质的积聚，并有利于LD表面TAG的合成。Elhan等人的研究表明，在脂滴生长过程中，ATG2A与生成三酰甘油（TAG）的酶DGAT2共同作用。通过将二酰基甘油输送到脂滴，ATG2A不仅为TAG的产生提供燃料，而且还促进DGAT2在脂滴表面的招募。
{"title":"ATG2A-mediated DAG transfer recruits DGAT2 for lipid droplet growth","authors":"Helin Elhan, Alicia Damm, Justin L. Korfhage, Daniel Álvarez, Mehdi Zouiouich, Francesca Giordano, Stefano Vanni, Thomas J. Melia, Abdou Rachid Thiam","doi":"10.1038/s41594-025-01689-0","DOIUrl":"10.1038/s41594-025-01689-0","url":null,"abstract":"Lipid droplet (LD) growth mechanisms and the roles of LD-associated lipid transfer proteins remain poorly understood. Here we show that the autophagy lipid transfer protein ATG2A has an anabolic role and promotes LD expansion by transferring diacylglycerol (DAG), triacylglycerol (TAG) and phosphatidic acid, from the endoplasmic reticulum to LDs. In ATG2A deficiency, synthesized lipids are incorporated inefficiently into LDs and assemble new LDs. In addition, DAG O-acyltransferase 2 (DGAT2), which synthesizes TAG and expands LD, fails to relocate to LDs. In vitro, DAG recruits DGAT2 to LDs. These findings support the idea that ATG2A-mediated DAG transfer recruits DGAT2 to LDs, promoting LD expansion. ATG2A alone promotes LD growth by transferring TAG and DAG, but its effectiveness in LD expansion is reduced when DGAT2 is inhibited. This synergistic action with DGAT2 prevents the buildup of nonmembrane lipids within the endoplasmic reticulum and favors TAG synthesis on the LD surface. Elhan et al. show that ATG2A acts with DGAT2, the enzyme producing triacylglycerol (TAG), in lipid droplet growth. By delivering diacylglycerol to lipid droplets, ATG2A not only fuels TAG production but also promotes the recruitment of DGAT2 to droplet surfaces.","PeriodicalId":49141,"journal":{"name":"Nature Structural & Molecular Biology","volume":"32 12","pages":"2601-2613"},"PeriodicalIF":10.1,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41594-025-01689-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145531500","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}
Pub Date : 2025-11-17DOI: 10.1038/s41594-025-01714-2
Li Mi, Yu-Xuan Li, Xinchen Lv, Zi-Li Wan, Xu Liu, Kairan Zhang, Huican Li, Yue Yao, Leping Zhang, Zhe Xu, Xingyu Zhuang, Kunqian Ji, Min Jiang, Yangming Wang, Peilong Lu
Bystander editing remains a major limitation of current base editors, hindering their precision and therapeutic potential. Here, we present a de novo protein design strategy that creates a structurally rigid interface between a DNA-binding TALE domain and a cytosine deaminase, forming a unified editing module termed TALE-oriented deaminase (TOD). Cryo-EM analysis of TOD–DNA complexes confirms that this precise spatial architecture tightly restricts the deaminase activity window, thereby minimizing unwanted deamination. To further enhance editing specificity, we develop a split version, termed DdCBE–TOD, which virtually eliminates off-target editing. As a proof of concept, we apply DdCBE–TOD to generate a mitochondrial disease mouse model and to correct a pathogenic mutation associated with MERRF syndrome in patient-derived cells, achieving single-nucleotide precision. This work introduces a generalizable and computationally guided approach for ultra-precise base editing, offering a promising platform for both mechanistic studies and therapeutic correction of single-nucleotide mutations. Mi et al. use de novo protein design to address bystander and off-target editing in base editing, resulting in a highly precise mitochondrial cytosine base editor that is valuable for studying and treating mitochondrial diseases.
{"title":"Computational design of a high-precision mitochondrial DNA cytosine base editor","authors":"Li Mi, Yu-Xuan Li, Xinchen Lv, Zi-Li Wan, Xu Liu, Kairan Zhang, Huican Li, Yue Yao, Leping Zhang, Zhe Xu, Xingyu Zhuang, Kunqian Ji, Min Jiang, Yangming Wang, Peilong Lu","doi":"10.1038/s41594-025-01714-2","DOIUrl":"10.1038/s41594-025-01714-2","url":null,"abstract":"Bystander editing remains a major limitation of current base editors, hindering their precision and therapeutic potential. Here, we present a de novo protein design strategy that creates a structurally rigid interface between a DNA-binding TALE domain and a cytosine deaminase, forming a unified editing module termed TALE-oriented deaminase (TOD). Cryo-EM analysis of TOD–DNA complexes confirms that this precise spatial architecture tightly restricts the deaminase activity window, thereby minimizing unwanted deamination. To further enhance editing specificity, we develop a split version, termed DdCBE–TOD, which virtually eliminates off-target editing. As a proof of concept, we apply DdCBE–TOD to generate a mitochondrial disease mouse model and to correct a pathogenic mutation associated with MERRF syndrome in patient-derived cells, achieving single-nucleotide precision. This work introduces a generalizable and computationally guided approach for ultra-precise base editing, offering a promising platform for both mechanistic studies and therapeutic correction of single-nucleotide mutations. Mi et al. use de novo protein design to address bystander and off-target editing in base editing, resulting in a highly precise mitochondrial cytosine base editor that is valuable for studying and treating mitochondrial diseases.","PeriodicalId":49141,"journal":{"name":"Nature Structural & Molecular Biology","volume":"32 12","pages":"2575-2586"},"PeriodicalIF":10.1,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145531501","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}
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