Pub Date : 2025-11-14DOI: 10.1016/j.ceb.2025.102599
Cassia Michael , Sofia de Oliveira
{"title":"Corrigendum to Exploring the dynamic behavior of leukocytes with zebrafish Curr Opin Cell Biol 85 December 2023 102276-","authors":"Cassia Michael , Sofia de Oliveira","doi":"10.1016/j.ceb.2025.102599","DOIUrl":"10.1016/j.ceb.2025.102599","url":null,"abstract":"","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"97 ","pages":"Article 102599"},"PeriodicalIF":4.3,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145528695","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}
Pub Date : 2025-11-08DOI: 10.1016/j.ceb.2025.102597
Jay T. Groves
The growing ease with which single molecules can be visualized in living systems is providing a fantastic new view into the molecular processes of cellular signal transduction. The single-molecule perspective reveals stochastic variation and molecular heterogeneity in unaveraged detail and is revealing new mechanisms by which biological functionality is physically achieved. Here we discuss several examples of newly emerging signaling mechanisms intrinsically rooted in the stochastic realm. The common theme is a competitive enzymatic reaction cycle with the substrate and product localized to the membrane, while the controlling enzymes reside in the cytosol. This general reaction configuration is extremely common among signaling systems, and some quite unexpected behaviors can be observed when the functional system includes only a small number of molecules.
{"title":"Single-molecule biophysics in signaling: Functionality from stochastic effects","authors":"Jay T. Groves","doi":"10.1016/j.ceb.2025.102597","DOIUrl":"10.1016/j.ceb.2025.102597","url":null,"abstract":"<div><div>The growing ease with which single molecules can be visualized in living systems is providing a fantastic new view into the molecular processes of cellular signal transduction. The single-molecule perspective reveals stochastic variation and molecular heterogeneity in unaveraged detail and is revealing new mechanisms by which biological functionality is physically achieved. Here we discuss several examples of newly emerging signaling mechanisms intrinsically rooted in the stochastic realm. The common theme is a competitive enzymatic reaction cycle with the substrate and product localized to the membrane, while the controlling enzymes reside in the cytosol. This general reaction configuration is extremely common among signaling systems, and some quite unexpected behaviors can be observed when the functional system includes only a small number of molecules.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"97 ","pages":"Article 102597"},"PeriodicalIF":4.3,"publicationDate":"2025-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145466280","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}
Pub Date : 2025-11-01DOI: 10.1016/j.ceb.2025.102596
Michelle F. Marchan , James E. Bear
Membrane trafficking is an essential aspect of cellular physiology, determining the spatial distribution of macromolecules within a cell in response to conditions such as nutrient availability and cellular stress. Much of this trafficking happens at intracellular membrane delimited vesicles and organelles—here referred to as endomembranes. Actin cytoskeletal dynamics contribute to intracellular force production, including fueling aspects of membrane trafficking on endomembranes. Cellular membrane trafficking and actin dynamics have traditionally been studied as separate specializations. Yet, actin networks interact with membranes and contribute to membrane remodeling, organelle motility, and cargo sorting. Here, we propose a conceptual framework for how actin filament networks participate in endomembrane trafficking and describe examples of each of the putative functions. Furthermore, we describe how aberrant actin-endomembrane interactions contribute to disease states and pose some open questions for the field.
{"title":"When two worlds collide: actin dynamics on endomembranes regulates membrane trafficking","authors":"Michelle F. Marchan , James E. Bear","doi":"10.1016/j.ceb.2025.102596","DOIUrl":"10.1016/j.ceb.2025.102596","url":null,"abstract":"<div><div>Membrane trafficking is an essential aspect of cellular physiology, determining the spatial distribution of macromolecules within a cell in response to conditions such as nutrient availability and cellular stress. Much of this trafficking happens at intracellular membrane delimited vesicles and organelles—here referred to as endomembranes. Actin cytoskeletal dynamics contribute to intracellular force production, including fueling aspects of membrane trafficking on endomembranes. Cellular membrane trafficking and actin dynamics have traditionally been studied as separate specializations. Yet, actin networks interact with membranes and contribute to membrane remodeling, organelle motility, and cargo sorting. Here, we propose a conceptual framework for how actin filament networks participate in endomembrane trafficking and describe examples of each of the putative functions. Furthermore, we describe how aberrant actin-endomembrane interactions contribute to disease states and pose some open questions for the field.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"97 ","pages":"Article 102596"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145417203","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}
Pub Date : 2025-10-16DOI: 10.1016/j.ceb.2025.102593
Fernando R. Valencia, Sergey V. Plotnikov
Mechanical forces shape cellular form and function by regulating key cellular processes; however, when dysregulated, they contribute to disease. Excessive forces can be detrimental to cells, damaging cytoskeleton, deforming nuclei, and even rupturing the cell itself. To counteract these effects, cells deploy protective mechanisms that enhance mechanical resilience. Emerging evidence highlights a novel strategy for rapid tension release via force-dependent actin polymerization mediated by formin-family proteins such as Dia1. Acting as a mechanical “safety valve”, Dia1 buffers otherwise damaging stress and promotes zyxin-mediated repair, preserving cytoskeletal architecture, safeguarding the nucleus, and maintaining cellular integrity. Loss of Dia1 disrupts signaling cascades that converge on key mechanotransduction processes governing cell fate and disease progression. In this review, we explore recent advances in force-dependent actin polymerization and its role in cytoskeletal protection, nuclear homeostasis, and cellular adaptation to mechanical forces.
{"title":"Actin cytoskeleton protection by the formin-mediated safety valve","authors":"Fernando R. Valencia, Sergey V. Plotnikov","doi":"10.1016/j.ceb.2025.102593","DOIUrl":"10.1016/j.ceb.2025.102593","url":null,"abstract":"<div><div>Mechanical forces shape cellular form and function by regulating key cellular processes; however, when dysregulated, they contribute to disease. Excessive forces can be detrimental to cells, damaging cytoskeleton, deforming nuclei, and even rupturing the cell itself. To counteract these effects, cells deploy protective mechanisms that enhance mechanical resilience. Emerging evidence highlights a novel strategy for rapid tension release via force-dependent actin polymerization mediated by formin-family proteins such as Dia1. Acting as a mechanical “safety valve”, Dia1 buffers otherwise damaging stress and promotes zyxin-mediated repair, preserving cytoskeletal architecture, safeguarding the nucleus, and maintaining cellular integrity. Loss of Dia1 disrupts signaling cascades that converge on key mechanotransduction processes governing cell fate and disease progression. In this review, we explore recent advances in force-dependent actin polymerization and its role in cytoskeletal protection, nuclear homeostasis, and cellular adaptation to mechanical forces.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"97 ","pages":"Article 102593"},"PeriodicalIF":4.3,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145318780","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}
Pub Date : 2025-10-13DOI: 10.1016/j.ceb.2025.102595
Tor Erik Rusten
The first identified regulators of autophagy were the hormones Glucagon and Insulin, long before the recognition that they act through receptor-mediated cell signaling pathways. More than two decades since the identification of the autophagy molecular machinery, we appreciate that regulation of autophagy is complex, operates at several levels, and serves many functions to maintain cellular and organismal health. TORC1 remains the best-defined gatekeeper, serving to sense nutrient and energy sufficiency while also integrating systemic growth factor signaling to control cell growth and autophagy autonomously. This review summarizes the current understanding of autophagy regulation by signaling through TORC1-dependent and independent mechanisms and discusses the emerging understanding of control and coordinated response of autophagy at the organism level.
{"title":"Autophagy regulation by signaling","authors":"Tor Erik Rusten","doi":"10.1016/j.ceb.2025.102595","DOIUrl":"10.1016/j.ceb.2025.102595","url":null,"abstract":"<div><div>The first identified regulators of autophagy were the hormones Glucagon and Insulin, long before the recognition that they act through receptor-mediated cell signaling pathways. More than two decades since the identification of the autophagy molecular machinery, we appreciate that regulation of autophagy is complex, operates at several levels, and serves many functions to maintain cellular and organismal health. TORC1 remains the best-defined gatekeeper, serving to sense nutrient and energy sufficiency while also integrating systemic growth factor signaling to control cell growth and autophagy autonomously. This review summarizes the current understanding of autophagy regulation by signaling through TORC1-dependent and independent mechanisms and discusses the emerging understanding of control and coordinated response of autophagy at the organism level.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"97 ","pages":"Article 102595"},"PeriodicalIF":4.3,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145294272","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}
The skin is a dynamic, regenerative organ capable of withstanding diverse internal and external stresses, supported by tissue-resident stem cells. A complex signaling network regulates interactions between epidermal stem cells, dermal cells, immune cells, and the extracellular matrix to maintain tissue integrity. Disruptions in these signaling pathways can impair cellular communication, alter stem cell lineage commitment, and compromise epidermal stem cell identity, ultimately resulting in a loss of coordinated tissue function. In this review, we highlight recent insights into three key signaling factors—metabolic, mechanical, and inflammatory cues—that regulate epidermal stem cell behavior during homeostasis, regeneration, and aging. We further discuss how dysregulation of these pathways contributes to pathological skin remodeling and explore emerging intervention strategies targeting signaling molecules to restore epidermal stem cell function and skin health.
{"title":"New insights into signaling networks coordinating epidermal stem cell regulation in skin regeneration and aging","authors":"Mizuho Ishikawa , Hung Manh Phung , Thisakorn Dumrongphuttidecha , Aiko Sada","doi":"10.1016/j.ceb.2025.102594","DOIUrl":"10.1016/j.ceb.2025.102594","url":null,"abstract":"<div><div>The skin is a dynamic, regenerative organ capable of withstanding diverse internal and external stresses, supported by tissue-resident stem cells. A complex signaling network regulates interactions between epidermal stem cells, dermal cells, immune cells, and the extracellular matrix to maintain tissue integrity. Disruptions in these signaling pathways can impair cellular communication, alter stem cell lineage commitment, and compromise epidermal stem cell identity, ultimately resulting in a loss of coordinated tissue function. In this review, we highlight recent insights into three key signaling factors—metabolic, mechanical, and inflammatory cues—that regulate epidermal stem cell behavior during homeostasis, regeneration, and aging. We further discuss how dysregulation of these pathways contributes to pathological skin remodeling and explore emerging intervention strategies targeting signaling molecules to restore epidermal stem cell function and skin health.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"97 ","pages":"Article 102594"},"PeriodicalIF":4.3,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253534","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}
Pub Date : 2025-10-01Epub Date: 2025-08-10DOI: 10.1016/j.ceb.2025.102578
G W Gant Luxton, Selin Gümüşderelioğlu, Kassandra M Ori-McKenney, Daniel A Starr, Richard J McKenney
Nuclear-cytoskeletal coupling orchestrates critical cellular processes from migration to tissue organization. At the core of this machinery, outer nuclear membrane Klarsicht/ANC-1/SYNE homology (KASH) proteins function as sophisticated molecular conductors rather than simple structural tethers. This review examines three principles redefining these versatile proteins: specialized interfaces for selective microtubule motor protein recruitment that orchestrate diverse chromosomal and nuclear dynamics, coordination of multiple cytoskeletal systems through simultaneous engagement with actin and microtubules, and tissue-specific regulation that explains the diverse KASH protein-related disease manifestations. This framework provides insights into conditions from muscular dystrophy to neurodegeneration and suggests targeted therapeutic opportunities.
核-细胞骨架耦合协调从迁移到组织组织的关键细胞过程。在这一机制的核心，外核膜Klarsicht/ ac -1/SYNE同源（KASH）蛋白是复杂的分子导体，而不是简单的结构绳索。这篇综述探讨了重新定义这些多功能蛋白的三个原则：选择性微管运动蛋白募集的专门界面，协调多种染色体和核动力学，通过同时参与肌动蛋白和微管来协调多个细胞骨架系统，以及解释多种KASH蛋白相关疾病表现的组织特异性调节。这个框架提供了从肌肉萎缩症到神经退行性疾病的见解，并提出了有针对性的治疗机会。
{"title":"KASH proteins transform from passive tethers to dynamic conductors of motor-driven nuclear dynamics.","authors":"G W Gant Luxton, Selin Gümüşderelioğlu, Kassandra M Ori-McKenney, Daniel A Starr, Richard J McKenney","doi":"10.1016/j.ceb.2025.102578","DOIUrl":"10.1016/j.ceb.2025.102578","url":null,"abstract":"<p><p>Nuclear-cytoskeletal coupling orchestrates critical cellular processes from migration to tissue organization. At the core of this machinery, outer nuclear membrane Klarsicht/ANC-1/SYNE homology (KASH) proteins function as sophisticated molecular conductors rather than simple structural tethers. This review examines three principles redefining these versatile proteins: specialized interfaces for selective microtubule motor protein recruitment that orchestrate diverse chromosomal and nuclear dynamics, coordination of multiple cytoskeletal systems through simultaneous engagement with actin and microtubules, and tissue-specific regulation that explains the diverse KASH protein-related disease manifestations. This framework provides insights into conditions from muscular dystrophy to neurodegeneration and suggests targeted therapeutic opportunities.</p>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"96 ","pages":"102578"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12581424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144823153","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}
Pub Date : 2025-10-01DOI: 10.1016/j.ceb.2025.102585
Benjamin Woodhams , Virginie Uhlmann
Deep learning (DL) has revolutionized bioimage analysis, enabling unprecedented insights into cellular dynamics. This review provides an overview of state-of-the-art DL approaches for quantifying cellular dynamics from 2D microscopy images, considering the three fundamental steps in dynamics analysis: identifying objects in space through segmentation, connecting them through time via tracking, and extracting meaningful measurements from their resulting trajectories. We highlight how recent methodological innovations in DL are complementing more classical, long-established algorithms, and discuss emerging trends as well as the importance of ensuring that DL-powered cellular dynamics analysis remains scientifically sound and accessible. By discussing methodological advances and pointing to available practical tools, this review aims to bridge the gap between computational expertise and biological applications, providing guidance to help navigate this rapidly evolving field and identify approaches that are relevant to specific research questions.
{"title":"From images to understanding: Advances in deep learning for cellular dynamics analysis","authors":"Benjamin Woodhams , Virginie Uhlmann","doi":"10.1016/j.ceb.2025.102585","DOIUrl":"10.1016/j.ceb.2025.102585","url":null,"abstract":"<div><div>Deep learning (DL) has revolutionized bioimage analysis, enabling unprecedented insights into cellular dynamics. This review provides an overview of state-of-the-art DL approaches for quantifying cellular dynamics from 2D microscopy images, considering the three fundamental steps in dynamics analysis: identifying objects in space through segmentation, connecting them through time via tracking, and extracting meaningful measurements from their resulting trajectories. We highlight how recent methodological innovations in DL are complementing more classical, long-established algorithms, and discuss emerging trends as well as the importance of ensuring that DL-powered cellular dynamics analysis remains scientifically sound and accessible. By discussing methodological advances and pointing to available practical tools, this review aims to bridge the gap between computational expertise and biological applications, providing guidance to help navigate this rapidly evolving field and identify approaches that are relevant to specific research questions.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"97 ","pages":"Article 102585"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145214123","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}
Cell competition is a fundamental mechanism of tissue quality control that enables the selective elimination of less fit, mis-specified, diseased or aged cells. By shaping tissue composition, it plays a critical role in development, organismal health and a wide range of physiological and pathological contexts, including cancer. As its biological significance continues to grow, elucidating the molecular mechanisms underlying cell competition is essential for advancing our understanding of tissue biology, disease progression and future therapeutic strategies. In this review, we highlight recently identified, evolutionarily conserved pathways that govern cell competition through metabolites and systemic signals, proteostasis and mechanical exchange. By integrating findings across species and pathways, we reveal how these distinct mechanisms may intersect and coordinate to determine competitive outcomes, providing a conceptual framework to inform and guide future research.
{"title":"Mechanisms of cellular fitness and cell competition: Towards an integrated view.","authors":"Jules Lavalou, Karyna Kulakova, Yogaspoorthi J Subramaniam, Eugenia Piddini","doi":"10.1016/j.ceb.2025.102571","DOIUrl":"10.1016/j.ceb.2025.102571","url":null,"abstract":"<p><p>Cell competition is a fundamental mechanism of tissue quality control that enables the selective elimination of less fit, mis-specified, diseased or aged cells. By shaping tissue composition, it plays a critical role in development, organismal health and a wide range of physiological and pathological contexts, including cancer. As its biological significance continues to grow, elucidating the molecular mechanisms underlying cell competition is essential for advancing our understanding of tissue biology, disease progression and future therapeutic strategies. In this review, we highlight recently identified, evolutionarily conserved pathways that govern cell competition through metabolites and systemic signals, proteostasis and mechanical exchange. By integrating findings across species and pathways, we reveal how these distinct mechanisms may intersect and coordinate to determine competitive outcomes, providing a conceptual framework to inform and guide future research.</p>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"96 ","pages":"102571"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144818112","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}
Pub Date : 2025-09-26DOI: 10.1016/j.ceb.2025.102583
Asma Majoul , Ana J. Garcia-Saez
There are many ways for a cell to die, but each cell only dies once, causing an inherent variability that results from common triggers activating interconnected signaling networks that diverge at key decision points during cell death initiation, progression, and execution. Despite the death of each cell being a unique biomolecular event, shared features allow us to categorize the process depending on the pathways activated and their outcomes. Here we outline core concepts about the dynamic interplay between cell death pathways, focusing on apoptosis, necroptosis, pyroptosis, and ferroptosis. We highlight unresolved decision points, including the dynamics of pore formation and the points of no return. We also discuss conceptual commonalities across systems and outline key recent developments that refine our understanding of the dynamic regulation of cell death.
{"title":"Dynamic regulation of cell death signaling","authors":"Asma Majoul , Ana J. Garcia-Saez","doi":"10.1016/j.ceb.2025.102583","DOIUrl":"10.1016/j.ceb.2025.102583","url":null,"abstract":"<div><div>There are many ways for a cell to die, but each cell only dies once, causing an inherent variability that results from common triggers activating interconnected signaling networks that diverge at key decision points during cell death initiation, progression, and execution. Despite the death of each cell being a unique biomolecular event, shared features allow us to categorize the process depending on the pathways activated and their outcomes. Here we outline core concepts about the dynamic interplay between cell death pathways, focusing on apoptosis, necroptosis, pyroptosis, and ferroptosis. We highlight unresolved decision points, including the dynamics of pore formation and the points of no return. We also discuss conceptual commonalities across systems and outline key recent developments that refine our understanding of the dynamic regulation of cell death.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"97 ","pages":"Article 102583"},"PeriodicalIF":4.3,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145159807","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}
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