Journal of Cell Biology最新文献_第7页

The Unkempt RNA-binding protein reveals a local translation program in centriole overduplication. Unkempt rna结合蛋白揭示了中心粒过度复制的局部翻译程序。

IF 6.4 1区生物学

Journal of Cell Biology Pub Date : 2025-08-04 Epub Date: 2025-07-23 DOI: 10.1083/jcb.202407196

Abraham Martinez, Alexander J Stemm-Wolf, Ryan M Sheridan, J Matthew Taliaferro, Chad G Pearson

{"title":"The Unkempt RNA-binding protein reveals a local translation program in centriole overduplication.","authors":"Abraham Martinez, Alexander J Stemm-Wolf, Ryan M Sheridan, J Matthew Taliaferro, Chad G Pearson","doi":"10.1083/jcb.202407196","DOIUrl":"10.1083/jcb.202407196","url":null,"abstract":"Excess centrosomes cause defects in mitosis, cell-signaling, and cell migration, and therefore their assembly is tightly regulated. The divergent Polo kinase, PLK4, controls centriole duplication at the heart of centrosome assembly, and elevated PLK4 levels promote centrosome amplification (CA), a founding event of tumorigenesis. Here, we investigate the transcriptional consequences of elevated PLK4 and find Unkempt (UNK), a gene encoding an RNA-binding protein with roles in mRNA translational regulation, to be one of only two upregulated mRNAs. UNK protein localizes around centrosomes and with CEP131-positive centriolar satellites, promoting CEP131 localization to and around centrosomes. UNK's RNA-binding activity is required for PLK4-induced centriole overduplication. Consistent with the loss in PLK4-induced centriole overduplication, UNK depletion disrupts PLK4 and centriole assembly protein localization. Finally, translation is enriched at centrosomes and centriolar satellites, with UNK and CEP131 promoting this localized translation. In summary, UNK and CEP131 promote PLK4 localization and local translation at centrosomes during centriole overduplication.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 8","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12286598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144690394","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

CNTD1 is crucial for crossover formation in female meiosis and for establishing the ovarian reserve. CNTD1在女性减数分裂的交叉形成和卵巢储备的建立中起着至关重要的作用。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-08-04 Epub Date: 2025-06-09 DOI: 10.1083/jcb.202401021

Anna J Wood, Rania M Ahmed, Leah E Simon, Rachel A Bradley, Stephen Gray, Ian D Wolff, Paula E Cohen

{"title":"CNTD1 is crucial for crossover formation in female meiosis and for establishing the ovarian reserve.","authors":"Anna J Wood, Rania M Ahmed, Leah E Simon, Rachel A Bradley, Stephen Gray, Ian D Wolff, Paula E Cohen","doi":"10.1083/jcb.202401021","DOIUrl":"10.1083/jcb.202401021","url":null,"abstract":"In meiotic prophase I, hundreds of DNA double-strand breaks are formed and subsequently repaired as noncrossovers or crossovers (COs). COs are essential for accurate chromosome segregation during the first meiotic division, and errors in this process result in aneuploidy, birth defects, or infertility. Such errors are more pronounced in females compared with males, indicating that CO regulation and surveillance are sexually dimorphic. We demonstrate here dual roles of cyclin N-terminal domain containing 1 (CNTD1) in ensuring appropriate CO between homologous chromosomes in oocytes and in establishing the pool of follicles in the postnatal ovary. CNTD1-deficient oocytes fail to form COs and exhibit a severely depleted follicle pool shortly after birth, which is temporally distinct from previously reported CO mutants. Further investigation indicates that follicle loss is CHK2-dependent, resulting from inappropriate retention of HORMAD1 and the absence of SKP1. These findings indicate that CNTD1 plays novel roles in CO designation and establishment of the follicular reserve in female mammals.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 8","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12147665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248073","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

B cell mechanotransduction via ATAT1 coordinates actin and lysosomal dynamics at the immune synapse. 通过ATAT1的B细胞机械转导协调免疫突触的肌动蛋白和溶酶体动力学。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-08-04 Epub Date: 2025-07-21 DOI: 10.1083/jcb.202506017

Srishti Mandal, Sudha Kumari

引用次数: 0

A substrate-interacting region of Parkin directs ubiquitination of the mitochondrial GTPase Miro1. Parkin的底物相互作用区域指导线粒体GTPase Miro1的泛素化。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-08-04 Epub Date: 2025-06-27 DOI: 10.1083/jcb.202408025

Joanna Koszela, Anne Rintala-Dempsey, Giulia Salzano, Viveka Pimenta, Outi Kamarainen, Mads Gabrielsen, Aasna L Parui, Gary S Shaw, Helen Walden

{"title":"A substrate-interacting region of Parkin directs ubiquitination of the mitochondrial GTPase Miro1.","authors":"Joanna Koszela, Anne Rintala-Dempsey, Giulia Salzano, Viveka Pimenta, Outi Kamarainen, Mads Gabrielsen, Aasna L Parui, Gary S Shaw, Helen Walden","doi":"10.1083/jcb.202408025","DOIUrl":"10.1083/jcb.202408025","url":null,"abstract":"Mutations in the E3 ubiquitin ligase Parkin gene have been linked to early onset Parkinson's disease. Besides many other roles, Parkin is involved in clearance of damaged mitochondria via mitophagy-a process of particular importance in dopaminergic neurons. Upon mitochondrial damage, Parkin accumulates at the outer mitochondrial membrane and is activated, leading to ubiquitination of many mitochondrial substrates and recruitment of mitophagy effectors. While the activation mechanisms of autoinhibited Parkin have been extensively studied, it remains unknown how Parkin recognizes its substrates for ubiquitination. Here, we characterize a conserved region in the flexible linker between the Ubl and RING0 domains of Parkin, which is indispensable for Parkin interaction with the mitochondrial GTPase Miro1. Our results may explain fast kinetics of Miro1 ubiquitination by Parkin in recombinant assays and provide a biochemical explanation for Miro1-dependent Parkin recruitment to the mitochondrial membrane observed in cells. Our findings are important for understanding mitochondrial homeostasis and may inspire new therapeutic avenues for Parkinson's disease.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 8","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505823","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

Arc spreads Crumbs: Spatial restriction of tissue invagination to form a thin epithelial tube. 弧形扩散碎屑：组织内陷的空间限制，形成薄上皮管。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-07-31 DOI: 10.1083/jcb.202507106

Tony J C Harris

引用次数: 0

The p97 ATPase and its adaptor UBXD8 maintain peroxisome pools by preventing pexophagy. p97 atp酶及其接头UBXD8通过防止噬酶来维持过氧化物酶体池。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-07-29 DOI: 10.1083/jcb.202409024

Iris D Montes,Suganthan Amirthagunanathan,Rakesh Ganji,Joao A Paulo,Brittany A Ahlstedt,Ly Nguyen,Amit S Joshi,Malavika Raman

{"title":"The p97 ATPase and its adaptor UBXD8 maintain peroxisome pools by preventing pexophagy.","authors":"Iris D Montes,Suganthan Amirthagunanathan,Rakesh Ganji,Joao A Paulo,Brittany A Ahlstedt,Ly Nguyen,Amit S Joshi,Malavika Raman","doi":"10.1083/jcb.202409024","DOIUrl":"https://doi.org/10.1083/jcb.202409024","url":null,"abstract":"Peroxisomes perform key metabolic functions in eukaryotic cells. Loss of peroxisome function causes peroxisome biogenesis disorders and severe childhood diseases with disrupted lipid metabolism. One mechanism regulating peroxisome abundance is degradation via selective autophagy (pexophagy). However, the mechanisms regulating pexophagy remain poorly understood in mammalian cells. Here, we find that the evolutionarily conserved AAA-ATPase p97/VCP and its adaptor UBXD8/FAF2 are essential for maintaining peroxisome abundance. From quantitative proteomics studies, we show that loss of UBXD8 affects the abundance of many peroxisomal proteins and that the depletion of UBXD8 results in a loss of peroxisomes. Loss of p97-UBXD8 and inhibition of p97 catalytic activity increase peroxisomal turnover through autophagy and can be rescued by depleting key autophagy proteins and E3 ligases or overexpressing the deubiquitylase USP30. We find increased ubiquitylation of PMP70 and PEX5 in cells lacking UBXD8 or p97. Our findings identify a new role of the p97-UBXD8 in regulating peroxisome abundance by removing ubiquitylated peroxisome membrane proteins to prevent pexophagy.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"5 1","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144720255","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

New insights into lipid droplet breakdown in alcohol-associated hepatic steatosis. 酒精相关性肝脂肪变性中脂滴分解的新见解

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-07-29 DOI: 10.1083/jcb.202506103

Chen Zhang,Wen-Xing Ding

引用次数: 0

FUT8-mediated core fucosylation stabilizes TMEM67 to promote ciliogenesis. fut8介导的核心聚焦稳定TMEM67促进纤毛发生。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-07-29 DOI: 10.1083/jcb.202412224

Difei Wang,Qingchao Li,Zhenqi Yu,Junkui Zhao,Mingzheng Hu,Xiaoshan Geng,Xinzhe Liu,Siyang Zhao,Ting Song,Min Liu,Dengwen Li,Huijie Zhao,Jun Zhou

{"title":"FUT8-mediated core fucosylation stabilizes TMEM67 to promote ciliogenesis.","authors":"Difei Wang,Qingchao Li,Zhenqi Yu,Junkui Zhao,Mingzheng Hu,Xiaoshan Geng,Xinzhe Liu,Siyang Zhao,Ting Song,Min Liu,Dengwen Li,Huijie Zhao,Jun Zhou","doi":"10.1083/jcb.202412224","DOIUrl":"https://doi.org/10.1083/jcb.202412224","url":null,"abstract":"Glycosylation of membrane proteins plays an essential role in diverse biological processes. However, it remains unknown whether this posttranslational modification occurs on ciliary membrane proteins. Herein, by mass spectrometry-based proteomic analysis, we demonstrate that multiple membrane proteins localized in the ciliary transition zone undergo core fucosylation, an N-linked glycosylation specifically catalyzed by fucosyltransferase 8 (FUT8). In-depth analysis reveals that FUT8 interacts with transmembrane protein 67 (TMEM67), a transition zone component closely linked to ciliopathies, and catalyzes its core fucosylation. Functional investigation shows that core fucosylation stabilizes TMEM67 by impeding its degradation via the autophagy pathway, thereby ensuring its proper localization to the transition zone to promote cilium formation. Fut8-deficient mice exhibit ciliary defects in multiple organs, such as the kidney, brain, and trachea. These findings uncover a critical role for TMEM67 core fucosylation in ciliogenesis and have important implications for the pathogenesis of ciliopathies.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"26 1","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144720350","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

An ethanol-induced loss of the lipid droplet-associated segregase VCP/p97 leads to hepatic steatosis. 乙醇引起的脂滴相关分离酶VCP/p97的丧失导致肝脏脂肪变性。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-07-29 DOI: 10.1083/jcb.202408205

Sandhya Sen,Shaun Weller,Ryan J Schulze,Donglin Ding,Carol A Casey,Conrad Weihl,Mark A McNiven

引用次数: 0

STIM-IP3R crosstalk regulates migration of breast cancer cells. STIM-IP3R串扰调控乳腺癌细胞的迁移。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-07-28 DOI: 10.1083/jcb.202411203

Ruslana Militsin,Hadas Achildiev Cohen,Maya Hershfinkel,Ofek Levi,Stavit Drori,Adi Yifat Raz,Yuval Shaked,Raz Palty

引用次数: 0