Journal of Cell Biology最新文献_第4页

Mechanical control of osteoclast fusion by membrane-cortex attachment and BAR proteins. 膜-皮质附着和BAR蛋白对破骨细胞融合的机械控制。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-05-08 DOI: 10.1083/jcb.202411024

Yumeng Wan,Yuri L Nemoto,Tsukasa Oikawa,Kazunori Takano,Takahiro K Fujiwara,Kazuya Tsujita,Toshiki Itoh

引用次数: 0

STIM1/2 maintain signaling competence at ER-PM contact sites during neutrophil spreading. STIM1/2在中性粒细胞扩散过程中维持ER-PM接触位点的信号传导能力。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-05-05 Epub Date: 2025-03-21 DOI: 10.1083/jcb.202406053

Camille Rabesahala de Meritens, Amado Carreras-Sureda, Nicolas Rosa, Robert Pick, Christoph Scheiermann, Nicolas Demaurex

{"title":"STIM1/2 maintain signaling competence at ER-PM contact sites during neutrophil spreading.","authors":"Camille Rabesahala de Meritens, Amado Carreras-Sureda, Nicolas Rosa, Robert Pick, Christoph Scheiermann, Nicolas Demaurex","doi":"10.1083/jcb.202406053","DOIUrl":"10.1083/jcb.202406053","url":null,"abstract":"Neutrophils are highly motile leukocytes that migrate inside tissues to destroy invading pathogens. Ca2+ signals coordinate leukocytes migration, but whether Ca2+ fluxes mediated by Stim proteins at ER-PM contact sites regulate neutrophil actin-based motility is unclear. Here, we show that myeloid-specific Stim1/2 ablation decreases basal cytosolic Ca2+ levels and prevents adhesion-induced Ca2+ elevations in mouse neutrophils, reducing actin fiber formation and impairing spreading. Unexpectedly, more ER-PM contact sites were detected on the actin-poor adhesive membranes of Stim1/2-deficient neutrophils, which had reduced inositol-1,4,5-trisphosphate receptor (IP3R) immunoreactivity on confocal and immunogold micrographs despite preserved IP3R levels on western blots. Remarkably, Stim1/2-deficient neutrophils regained signaling and spreading competence in Ca2+-rich solutions and were recruited more effectively in mouse inflamed cremaster muscles in vivo. Our findings indicate that Stim1/2 preserve IP3R functionality in neutrophils, generating adhesion-dependent Ca2+ signals that control actin dynamics during neutrophil spreading. Stim proteins thus maintain IP3R signaling competence at adhesive membranes, enabling Ca2+-dependent actin remodeling during spreading in mouse neutrophils.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 5","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11927589/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673466","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

Acetic acid-induced stress granules function as scaffolding complexes for Hog1 activation by Pbs2. 醋酸诱导的应激颗粒是Pbs2激活Hog1的支架复合物。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-05-05 Epub Date: 2025-03-11 DOI: 10.1083/jcb.202409072

Jongmin Lee, Kazuo Tatebayashi, David E Levin

引用次数: 0

Ceramide mediates cell-to-cell ER stress transmission by modulating membrane fluidity. 神经酰胺通过调节膜流动性介导细胞间内质网应力传递。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-05-05 Epub Date: 2025-03-26 DOI: 10.1083/jcb.202405060

Yazhen Huo, Xinlu Liu, Chen Lu, Tao Li, Zaili Yang, Fenfen Xu, Si Chen, Kailin Yin, Likun Wang

{"title":"Ceramide mediates cell-to-cell ER stress transmission by modulating membrane fluidity.","authors":"Yazhen Huo, Xinlu Liu, Chen Lu, Tao Li, Zaili Yang, Fenfen Xu, Si Chen, Kailin Yin, Likun Wang","doi":"10.1083/jcb.202405060","DOIUrl":"10.1083/jcb.202405060","url":null,"abstract":"Under endoplasmic reticulum (ER) stress (ERS), cells initiate the unfolded protein response (UPR) to maintain ER homeostasis. Recent studies revealed ERS transmission between cells and tissues, by activating the cell-nonautonomous UPR in cells that do not experience ERS directly. Here, we report that ERS triggers a rapid release of ceramide independent of the UPR, but requiring the acid sphingomyelinase activity. Carried by lipoproteins, ceramide is delivered to receiving cells to induce the UPR and regulate cell functions at multiple aspects, including lipid accumulation, cell death, and cytokine production. Mechanistically, extracellular ceramide stimulates ceramide synthesis at the transcription level in receiving cells, leading to ceramide accumulation in the ER so as to reduce membrane fluidity to disrupt ER calcium homeostasis, thus activating the UPR. Sphingomyelin counterbalanced the effect of ceramide. UPR induction is the frontline response to protect cells from ceramide insult. Our study suggests ceramide-mediated ERS transmission as a universal cell-cell communication model regulating a wide range of physiological events.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 5","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11938942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709927","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

Interactions with multiple inner kinetochore proteins determine mitotic localization of FACT. 与多个内着丝点蛋白的相互作用决定了FACT的有丝分裂定位。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-05-05 Epub Date: 2025-03-17 DOI: 10.1083/jcb.202412042

Julia Schweighofer, Bhagyashree Mulay, Ingrid Hoffmann, Doro Vogt, Marion E Pesenti, Andrea Musacchio

{"title":"Interactions with multiple inner kinetochore proteins determine mitotic localization of FACT.","authors":"Julia Schweighofer, Bhagyashree Mulay, Ingrid Hoffmann, Doro Vogt, Marion E Pesenti, Andrea Musacchio","doi":"10.1083/jcb.202412042","DOIUrl":"10.1083/jcb.202412042","url":null,"abstract":"The FAcilitates Chromatin Transcription (FACT) complex is a dimeric histone chaperone that operates on chromatin during transcription and replication. FACT also interacts with a specialized centromeric nucleosome containing the histone H3 variant centromere protein A (CENP-A) and with CENP-TW, two subunits of the constitutive centromere-associated network (CCAN), a 16-protein complex associated with CENP-A. The significance of these interactions remains elusive. Here, we show that FACT has multiple additional binding sites on CCAN. The interaction with CCAN is strongly stimulated by casein kinase II phosphorylation of FACT. Mitotic localization of FACT to kinetochores is strictly dependent on specific CCAN subcomplexes. Conversely, CENP-TW requires FACT for stable localization. Unexpectedly, we also find that DNA readily displaces FACT from CCAN, supporting the speculation that FACT becomes recruited through a pool of CCAN that is not stably integrated into chromatin. Collectively, our results point to a potential role of FACT in chaperoning CCAN during transcription or in the stabilization of CCAN at the centromere during the cell cycle.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 5","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912937/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648577","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

Cell signaling facilitates apical constriction by basolaterally recruiting Arp2/3 via Rac and WAVE. 细胞信号通过Rac和WAVE向基底侧募集Arp2/3促进根尖收缩。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-05-05 Epub Date: 2025-03-05 DOI: 10.1083/jcb.202409133

Pu Zhang, Taylor N Medwig-Kinney, Eleanor A Breiner, Jadyn M Perez, April N Song, Bob Goldstein

{"title":"Cell signaling facilitates apical constriction by basolaterally recruiting Arp2/3 via Rac and WAVE.","authors":"Pu Zhang, Taylor N Medwig-Kinney, Eleanor A Breiner, Jadyn M Perez, April N Song, Bob Goldstein","doi":"10.1083/jcb.202409133","DOIUrl":"10.1083/jcb.202409133","url":null,"abstract":"Apical constriction is a critical cell shape change that drives cell internalization and tissue bending. How precisely localized actomyosin regulators drive apical constriction remains poorly understood. Caenorhabditis elegans gastrulation provides a valuable model to address this question. The Arp2/3 complex is essential in C. elegans gastrulation. To understand how Arp2/3 is locally regulated, we imaged embryos with endogenously tagged Arp2/3 and its nucleation-promoting factors (NPFs). The three NPFs-WAVE, WASP, and WASH-controlled Arp2/3 localization at distinct subcellular locations. We exploited this finding to study distinct populations of Arp2/3 and found that only WAVE depletion caused penetrant gastrulation defects. WAVE localized basolaterally with Arp2/3 and controlled F-actin levels near cell-cell contacts. WAVE and Arp2/3 localization depended on CED-10/Rac. Establishing ectopic cell contacts recruited WAVE and Arp2/3, identifying the contact as a symmetry-breaking cue for localization of these proteins. These results suggest that cell-cell signaling via Rac activates WAVE and Arp2/3 basolaterally and that basolateral Arp2/3 makes an important contribution to apical constriction.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 5","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893165/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556962","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

Dock1 functions in Schwann cells to regulate development, maintenance, and repair. Dock1在雪旺细胞中起调节发育、维持和修复的作用。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-05-05 Epub Date: 2025-03-19 DOI: 10.1083/jcb.202311041

Ryan A Doan, Kelly R Monk

引用次数: 0

TANGO2 is an acyl-CoA binding protein. TANGO2是一种酰基辅酶a结合蛋白。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-05-05 Epub Date: 2025-02-27 DOI: 10.1083/jcb.202410001

Agustin Leonardo Lujan, Ombretta Foresti, Jose Wojnacki, Gonzalo Bigliani, Nathalie Brouwers, Maria Jesus Pena, Stefania Androulaki, Tomomi Hashidate-Yoshida, Maria Kalyukina, Sergey S Novoselov, Hideo Shindou, Vivek Malhotra

引用次数: 0

Ca2+ binding to Esyt modulates membrane contact site density in Drosophila photoreceptors. Ca2+结合Esyt调节果蝇光感受器膜接触位点密度。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-05-05 Epub Date: 2025-03-05 DOI: 10.1083/jcb.202407190

Vaisaly R Nath, Harini Krishnan, Shirish Mishra, Padinjat Raghu

引用次数: 0

Epigenetic deprogramming by disruption of CIZ1-RNA nuclear assemblies in early-stage breast cancers. 通过破坏早期乳腺癌中CIZ1-RNA核组装的表观遗传去编程。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-05-05 Epub Date: 2025-03-11 DOI: 10.1083/jcb.202409123

Gabrielle L Turvey, Ernesto López de Alba, Emma Stewart, Heather Cook, Ahmad Alalti, Richard T Gawne, Justin F-X Ainscough, Andrew S Mason, Dawn Coverley

{"title":"Epigenetic deprogramming by disruption of CIZ1-RNA nuclear assemblies in early-stage breast cancers.","authors":"Gabrielle L Turvey, Ernesto López de Alba, Emma Stewart, Heather Cook, Ahmad Alalti, Richard T Gawne, Justin F-X Ainscough, Andrew S Mason, Dawn Coverley","doi":"10.1083/jcb.202409123","DOIUrl":"10.1083/jcb.202409123","url":null,"abstract":"CIZ1 is part of the RNA-dependent supramolecular assemblies that form around the inactive X-chromosome (Xi) in female cells and smaller assemblies throughout the nucleus in both sexes. Here, we show that CIZ1 C-terminal anchor domain (AD) is elevated in human breast tumor transcriptomes, even at stage I. Elevation correlates with deprotection of chromatin and upregulation of lncRNA-containing gene clusters in ∼10 Mb regions enriched in cancer-associated genes. We modeled the effect of AD on endogenous CIZ1-Xi assemblies and observed dominant-negative interference with their reformation after mitosis, leading to abnormal assemblies similar to those in breast cancer cells, and depletion of H2AK119ub1, H3K27me3, and Xist. Consistent alterations in gene expression were evident across the genome, showing that AD-mediated interference has a destabilizing effect, likely by unscheduled exposure of underlying chromatin to modifying enzymes. The data argue for a dominant, potent, and rapid effect of CIZ1 AD that can deprogram gene expression patterns and which may predispose incipient tumors to epigenetic instability.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 5","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11895699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143605050","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