Journal of Cell Biology最新文献_第4页

Mechanical forces stimulate Golgi export. 机械力刺激高尔基输出。

IF 6.1 1区生物学

Journal of Cell Biology Pub Date : 2026-10-05 Epub Date: 2026-07-27 DOI: 10.1083/jcb.202510026

Chandini Bhaskar Naidu, Javier Vera Lillo, Eugenia Almacellas, Anabel-Lise Le Roux, Sabine Bardin, Nicolas Mateos, Jessica Angulo-Capel, Adam Wolowczyk, Yugo Terashima, Yuichi Wakana, Pere Roca-Cusachs, Maria F Garcia-Parajo, Franck Perez, Bruno Goud, Jean-Baptiste Manneville, Stéphanie Miserey, Felix Campelo

{"title":"Mechanical forces stimulate Golgi export.","authors":"Chandini Bhaskar Naidu, Javier Vera Lillo, Eugenia Almacellas, Anabel-Lise Le Roux, Sabine Bardin, Nicolas Mateos, Jessica Angulo-Capel, Adam Wolowczyk, Yugo Terashima, Yuichi Wakana, Pere Roca-Cusachs, Maria F Garcia-Parajo, Franck Perez, Bruno Goud, Jean-Baptiste Manneville, Stéphanie Miserey, Felix Campelo","doi":"10.1083/jcb.202510026","DOIUrl":"10.1083/jcb.202510026","url":null,"abstract":"Cells face diverse mechanical stimuli that vary with cell type, state, and pathological conditions. Mechanobiology investigates how cells sense and respond to these forces. While most work has focused on the cell surface and nucleus as primary mechanosensors, how intracellular organelles adapt to extracellular mechanical forces remains largely unknown. Here, we show that extracellular mechanical signals influence the secretory function of the Golgi apparatus. By subjecting adherent cells to mechanical challenges-cell spreading on different ligands, altered substrate stiffness, or equibiaxial strain-we reveal that extracellular forces modulate Golgi-to-cell surface carrier biogenesis, thereby regulating exocytosis. Together with changes in Golgi membrane tension, we identify molecular determinants of the mechanotransduction pathway, including microtubule acetylation, diacylglycerol production, and protein kinase D activity. In turn, inhibition of Golgi export suppresses this mechanoresponse and causes impaired cell spreading. These findings uncover a bidirectional mechanotransduction axis in which extracellular mechanics tune Golgi secretory output, providing a framework for investigating organelle-based mechanoadaptation in physiology and disease.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"225 10","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13404088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148591440","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}

引用次数: 0

Perturbation of nuclear proteins by optogenetic trapping in Drosophila ovary. 光遗传诱捕对果蝇卵巢核蛋白的扰动。

IF 6.1 1区生物学

Journal of Cell Biology Pub Date : 2026-10-05 Epub Date: 2026-08-19 DOI: 10.1083/jcb.202511189

Bing Liu, Aurelien Guillou, Sijia Zhou, Hao Li, Yaru Kong, Jiaying Liu, Denis Jullien, Thomas Mangeat, Luisa Di Stefano, Xiaobo Wang

{"title":"Perturbation of nuclear proteins by optogenetic trapping in Drosophila ovary.","authors":"Bing Liu, Aurelien Guillou, Sijia Zhou, Hao Li, Yaru Kong, Jiaying Liu, Denis Jullien, Thomas Mangeat, Luisa Di Stefano, Xiaobo Wang","doi":"10.1083/jcb.202511189","DOIUrl":"https://doi.org/10.1083/jcb.202511189","url":null,"abstract":"The eukaryotic nucleus hosts transcription factors and other numerous nuclear proteins essential for genome organization and function. Optogenetic tools have been applied to match nuclear protein dynamics but remain largely confined to transcription factors, leaving most nuclear proteins inaccessible for precise manipulation. Here, we engineered an optogenetic tool, nuclear localization sequence (NLS)-light-activated reversible inhibition by assembled trap (LARIAT), by fusing a NLS to LARIAT, enabling light-inducible clustering of diverse GFP-tagged nuclear proteins in Drosophila ovarian cells. NLS-LARIAT-mediated clustering of GFP-tagged transcriptional and epigenetic regulators, such as slow border cells (Slbo) and LSD1, phenocopied genetic inhibition while revealing rapid and localized roles of Slbo during border cell migration. Beyond regulatory factors, NLS-LARIAT can also be used to manipulate GFP-tagged nuclear structures, including the nuclear envelope and chromatin. Thus, NLS-LARIAT provides a versatile and broadly applicable optogenetic platform for spatiotemporal control of GFP-tagged nuclear proteins, offering new opportunities to dissect nuclear organization and function across model systems.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"225 10","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148793103","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}

引用次数: 0

Dysfunction of caveolae in muscle disease: A cell biological perspective. 肌肉疾病中的小泡功能障碍：细胞生物学的观点。

IF 6.1 1区生物学

Journal of Cell Biology Pub Date : 2026-10-05 Epub Date: 2026-09-09 DOI: 10.1083/jcb.202605101

Harriet P Lo, Stéphane Vassilopoulos, Nicholas Ariotti, Thomas E Hall, Robert G Parton

{"title":"Dysfunction of caveolae in muscle disease: A cell biological perspective.","authors":"Harriet P Lo, Stéphane Vassilopoulos, Nicholas Ariotti, Thomas E Hall, Robert G Parton","doi":"10.1083/jcb.202605101","DOIUrl":"https://doi.org/10.1083/jcb.202605101","url":null,"abstract":"Caveolae represent a prominent class of specialized membrane microdomains that are an abundant and striking feature of the sarcolemma of muscle cells. Loss or dysfunction of skeletal muscle caveolae can cause a spectrum of muscle diseases, including caveolinopathies associated with rippling muscle disease. Despite recent advances, the precise downstream mechanisms that link caveolar defects to muscle dysfunction are not resolved. In this review, we discuss the fundamental cell biology underpinning muscle diseases associated with caveolar disruption. We highlight how recent structural and functional advances in both muscle and non-muscle systems are providing crucial insights into these pathological processes. Specifically, we analyze how the loss of these abundant surface domains disrupts mechanoprotection, signal transduction, nanoscale lipid organization, and T-tubule biogenesis and function. Finally, we propose a unifying cell biological classification system for disease-associated variants of caveolin-3, with a view to providing a mechanistic framework to connect molecular defects with clinical phenotypes.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"225 10","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148912083","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}

引用次数: 0

Esc1-mediated anchoring regulates telomere clustering in response to metabolic changes. esc1介导的锚定调节端粒聚集响应代谢变化。

IF 6.1 1区生物学

Journal of Cell Biology Pub Date : 2026-10-05 Epub Date: 2026-08-12 DOI: 10.1083/jcb.202512168

Myriam Ruault, Isabelle Loïodice, Bradley D Keister, Antoine Even, Mickaël Garnier, Manuela Baquero-Pérez, David Waterman, James E Haber, Krastan B Blagoev, Vittore F Scolari, Angela Taddei

{"title":"Esc1-mediated anchoring regulates telomere clustering in response to metabolic changes.","authors":"Myriam Ruault, Isabelle Loïodice, Bradley D Keister, Antoine Even, Mickaël Garnier, Manuela Baquero-Pérez, David Waterman, James E Haber, Krastan B Blagoev, Vittore F Scolari, Angela Taddei","doi":"10.1083/jcb.202512168","DOIUrl":"https://doi.org/10.1083/jcb.202512168","url":null,"abstract":"Spatial organization of budding yeast telomeres is highly dynamic and regulated by growth conditions. In rich medium, the 32 telomeres group in 3-5 perinuclear foci, whereas they assemble into a hypercluster located in the center of the nucleus in long-lived quiescent (Q) cells, contributing to their long-term viability. Here, we explore the mechanisms underlying this reorganization. We rule out Sir3-mediated changes in telomere-telomere interactions as the main driver of hypercluster formation. Instead, physical modeling predicts that telomere anchoring antagonizes telomere clustering. Consistent with this prediction, genetic analyses support a model in which telomere anchoring relies on two redundant pathways in rich medium. One depends on PKA activity and is rapidly inactivated upon glucose depletion, whereas the other is progressively lost during entry into quiescence via dephosphorylation of a single residue of the nuclear envelope-associated protein Esc1. Inactivation of both pathways releases telomeres from the nuclear envelope, resulting in hypercluster formation specifically in Q cells.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"225 10","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148712329","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}

引用次数: 0

Characterizing the membrane recruitment domain of BDCPs and its role in gray platelet syndrome. bdcp的膜募集结构域特征及其在灰色血小板综合征中的作用。

IF 6.1 1区生物学

Journal of Cell Biology Pub Date : 2026-10-05 Epub Date: 2026-08-06 DOI: 10.1083/jcb.202510098

Anette Kathinka Dahl, Daniel Mann, Alf Håkon Lystad, Carsten Sachse, Anne Simonsen, Serhiy Pankiv

引用次数: 0

Ceramide transfer protein regulates G-protein-coupled phospholipase signalling in photoreceptors. 神经酰胺传递蛋白调控光感受器中g蛋白偶联磷脂酶信号。

IF 6.1 1区生物学

Journal of Cell Biology Pub Date : 2026-10-05 Epub Date: 2026-09-01 DOI: 10.1083/jcb.202511193

Shirish Mishra, Ali Khan, Vaisaly R Nath, Tejaswini Manoj, Thejaswini Balavali Gangadhar, Preethi Alex, Amruta Naik, Ujjaini Dasgupta, Padinjat Raghu

{"title":"Ceramide transfer protein regulates G-protein-coupled phospholipase signalling in photoreceptors.","authors":"Shirish Mishra, Ali Khan, Vaisaly R Nath, Tejaswini Manoj, Thejaswini Balavali Gangadhar, Preethi Alex, Amruta Naik, Ujjaini Dasgupta, Padinjat Raghu","doi":"10.1083/jcb.202511193","DOIUrl":"https://doi.org/10.1083/jcb.202511193","url":null,"abstract":"Non-vesicular lipid transfer at membrane contact sites (MCS) is proposed as a key principle in eukaryotic cells. While several lipid transfer proteins (LTPs) are localized at MCS, their physiological significance is poorly understood. Ceramide transfer protein (CERT) transfers ceramide between membranes in vitro. However, evidence for the in vivo significance of CERT function is limited. We find that loss of dcert, the only gene encoding CERT in Drosophila, results in elevated levels of short-chain ceramides along with reductions in the levels of its metabolite phosphoethanolamine ceramide in photoreceptors. Physiological analysis showed a reduced electrical response to light stimulation in dcert mutants. dcert mutants showed a reduction in the rate of phosphatidylinositol 4,5-bisphosphate (PIP2) resynthesis following light-induced phospholipase C (PLC) stimulation, associated with reduced ER-plasma membrane MCS density and function of the MCS-localized protein RDGB. Together, our findings suggest that CERT function regulates G-protein-coupled PLC signalling through modulation of MCS function in vivo.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"225 10","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872918","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}

引用次数: 0

Integrins and tetraspanins mediate CD36-actin coupling and regulate CD36 organization and signaling. 整合素和四跨蛋白介导CD36-肌动蛋白偶联并调节CD36的组织和信号传导。

IF 6.1 1区生物学

Journal of Cell Biology Pub Date : 2026-10-05 Epub Date: 2026-08-21 DOI: 10.1083/jcb.202504156

Soma Jana, Huong-Tra Ngo, Han Huang, Jaime Guerrero, Jesus Vega-Lugo, Nicolas Touret, Aparajita Dasgupta, Khuloud Jaqaman

{"title":"Integrins and tetraspanins mediate CD36-actin coupling and regulate CD36 organization and signaling.","authors":"Soma Jana, Huong-Tra Ngo, Han Huang, Jaime Guerrero, Jesus Vega-Lugo, Nicolas Touret, Aparajita Dasgupta, Khuloud Jaqaman","doi":"10.1083/jcb.202504156","DOIUrl":"https://doi.org/10.1083/jcb.202504156","url":null,"abstract":"Submembrane cortical actin (CA) plays a large role in regulating the dynamic organization of cell surface receptors, which in turn regulates receptor signaling. Many receptors have short intracellular domains and no known link to actin. Here, we identified the β1-integrin subunit and several tetraspanins (CD9, CD81, and CD151) as part of the hitherto unknown molecular link between the receptor CD36 and CA. Our data indicate that CD36 in vascular endothelial cells interacts with these proteins, with stronger interactions near the cell edge. Compromising these interactions via the point mutation G12V in the N-terminal transmembrane domain of CD36 alters the dynamic organization of CD36 on the cell surface and weakens its coupling to CA dynamics. Moreover, it abolishes thrombospondin-1-induced CD36 signaling through the Src family kinase Fyn. Given their many interactions with transmembrane proteins, tetraspanins and integrins may provide a ubiquitous mechanism for plasma membrane-CA coupling.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"225 10","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13496012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148793726","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}

引用次数: 0

Mammalian metaphase kinetochores are elastic and require condensin for robust structure and function. 哺乳动物中期着丝点是有弹性的，需要凝缩蛋白来维持坚固的结构和功能。

IF 6.1 1区生物学

Journal of Cell Biology Pub Date : 2026-10-05 Epub Date: 2026-08-25 DOI: 10.1083/jcb.202512154

Vanna M Tran, Jinghui Tao, Caleb J Rux, David Gomez Siu, Miquel Rosas-Salvans, Sophie Dumont

{"title":"Mammalian metaphase kinetochores are elastic and require condensin for robust structure and function.","authors":"Vanna M Tran, Jinghui Tao, Caleb J Rux, David Gomez Siu, Miquel Rosas-Salvans, Sophie Dumont","doi":"10.1083/jcb.202512154","DOIUrl":"10.1083/jcb.202512154","url":null,"abstract":"The mammalian kinetochore connects chromosomes to dynamic spindle microtubules. To remain attached, it must maintain structural integrity under force, but to what extent and how it does so remain unclear. Under spindle forces, we find using super-resolution microscopy that inner (CENP-A) and outer (Hec1) metaphase kinetochores undergo correlated, large-scale (1 µm) deformations along the force axis, suggesting dynamic, relative sliding of parallel protein linkages. Kinetochore shape changes can be asymmetric, with centromere-facing \"tails\" correlating with hyperstabilized microtubule attachments. Applying microneedle pulling forces, we demonstrate that kinetochores are elastic, stretching under force and relaxing in seconds afterward. Finally, we show that SMC2 depletion results in more variable kinetochore deformations, despite maintained elasticity, and in reduced microtubule attachment stability. Thus, the kinetochore is structurally highly dynamic, requiring a stable centromere base to maintain structure and function under force. We propose a model whereby individual protein linkages are stiff, yet global kinetochore structure is flexible to accommodate different attachment geometries and forces while maintaining function.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"225 10","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148813033","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}

引用次数: 0

Distinct mechanical regulation of PFK1 isoforms during cytoskeletal remodeling 细胞骨架重塑过程中PFK1亚型的独特机械调节

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2026-10-05 DOI: 10.1083/jcb.202512133

Logan W. Dawson,Nicholas M. Cronin,Corentin C.G. Charles,Mallory R. Tollefson,Megan C. Latham,Kris A. DeMali

{"title":"Distinct mechanical regulation of PFK1 isoforms during cytoskeletal remodeling","authors":"Logan W. Dawson,Nicholas M. Cronin,Corentin C.G. Charles,Mallory R. Tollefson,Megan C. Latham,Kris A. DeMali","doi":"10.1083/jcb.202512133","DOIUrl":"https://doi.org/10.1083/jcb.202512133","url":null,"abstract":"All cells experience mechanical forces that shape their behavior and organization. These forces are sensed at cell–cell adhesions and transduced through the actin cytoskeleton, triggering cytoskeletal reinforcement to withstand mechanical load. Such remodeling is energy-intensive and supported by increased glycolysis, yet the mechanisms linking mechanical stress to metabolic activation remain incomplete. Here, we identify phosphofructokinase-1 (PFK1) as a bridge coupling mechanotransduction and metabolism. Shear stress activates PFK1 and promotes its association with F-actin, enhancing reinforcement, glucose uptake, and intracellular ATP generation. Among the three human PFK1 isoforms, only the muscle isoform (PFKM) is essential for this response. The PFKM C-terminal tail is required for complete actin engagement and mechanosensitive activation: deletion abolishes this function, while grafting the tail onto other isoforms restores it. These findings establish PFKM as a mechanosensitive metabolic enzyme that links cytoskeletal mechanics to energy production, providing a framework for how mechanical and metabolic dysfunctions intersect in disease.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"8 1","pages":""},"PeriodicalIF":7.8,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149090097","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}

引用次数: 0

Stretching the secretory pathway: Mechanical control of Golgi export. 伸展分泌通路：高尔基出口的机械控制。

IF 6.1 1区生物学

Journal of Cell Biology Pub Date : 2026-10-05 Epub Date: 2026-09-03 DOI: 10.1083/jcb.202608044

Angelika Hausser

引用次数: 0