Journal of Cell Biology最新文献_第10页

Coordination of actin plus-end dynamics by IQGAP1, formin, and capping protein. IQGAP1、甲形蛋白和封顶蛋白对肌动蛋白加端动态的协调作用。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2024-09-02 Epub Date: 2024-05-24 DOI: 10.1083/jcb.202305065

Morgan L Pimm, Brian K Haarer, Alexander D Nobles, Laura M Haney, Alexandra G Marcin, Marcela Alcaide Eligio, Jessica L Henty-Ridilla

{"title":"Coordination of actin plus-end dynamics by IQGAP1, formin, and capping protein.","authors":"Morgan L Pimm, Brian K Haarer, Alexander D Nobles, Laura M Haney, Alexandra G Marcin, Marcela Alcaide Eligio, Jessica L Henty-Ridilla","doi":"10.1083/jcb.202305065","DOIUrl":"10.1083/jcb.202305065","url":null,"abstract":"Cell processes require precise regulation of actin polymerization that is mediated by plus-end regulatory proteins. Detailed mechanisms that explain plus-end dynamics involve regulators with opposing roles, including factors that enhance assembly, e.g., the formin mDia1, and others that stop growth (capping protein, CP). We explore IQGAP1's roles in regulating actin filament plus-ends and the consequences of perturbing its activity in cells. We confirm that IQGAP1 pauses elongation and interacts with plus ends through two residues (C756 and C781). We directly visualize the dynamic interplay between IQGAP1 and mDia1, revealing that IQGAP1 displaces the formin to influence actin assembly. Using four-color TIRF, we show that IQGAP1's displacement activity extends to formin-CP \"decision complexes,\" promoting end-binding protein turnover at plus-ends. Loss of IQGAP1 or its plus-end activities disrupts morphology and migration, emphasizing its essential role. These results reveal a new role for IQGAP1 in promoting protein turnover on filament ends and provide new insights into how plus-end actin assembly is regulated in cells.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":7.8,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11117073/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141086304","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

EVs move messes, not messages, at the synapse. 在突触中，EV 移动的是混乱，而不是信息。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2024-09-02 Epub Date: 2024-08-13 DOI: 10.1083/jcb.202408028

Marina N Bostelman, Heather T Broihier

引用次数: 0

AI analysis of super-resolution microscopy: Biological discovery in the absence of ground truth. 超分辨率显微镜的人工智能分析：在缺乏地面实况的情况下发现生物。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2024-08-05 Epub Date: 2024-06-12 DOI: 10.1083/jcb.202311073

Ivan R Nabi, Ben Cardoen, Ismail M Khater, Guang Gao, Timothy H Wong, Ghassan Hamarneh

引用次数: 0

Centrosome age breaks spindle size symmetry even in cells thought to divide symmetrically. 即使在被认为是对称分裂的细胞中，中心体的年龄也会打破纺锤体大小的对称性。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2024-08-05 Epub Date: 2024-07-16 DOI: 10.1083/jcb.202311153

Alexandre Thomas, Patrick Meraldi

{"title":"Centrosome age breaks spindle size symmetry even in cells thought to divide symmetrically.","authors":"Alexandre Thomas, Patrick Meraldi","doi":"10.1083/jcb.202311153","DOIUrl":"10.1083/jcb.202311153","url":null,"abstract":"Centrosomes are the main microtubule-organizing centers in animal cells. Due to the semiconservative nature of centrosome duplication, the two centrosomes differ in age. In asymmetric stem cell divisions, centrosome age can induce an asymmetry in half-spindle lengths. However, whether centrosome age affects the symmetry of the two half-spindles in tissue culture cells thought to divide symmetrically is unknown. Here, we show that in human epithelial and fibroblastic cell lines centrosome age imposes a mild spindle asymmetry that leads to asymmetric cell daughter sizes. At the mechanistic level, we show that this asymmetry depends on a cenexin-bound pool of the mitotic kinase Plk1, which favors the preferential accumulation on old centrosomes of the microtubule nucleation-organizing proteins pericentrin, γ-tubulin, and Cdk5Rap2, and microtubule regulators TPX2 and ch-TOG. Consistently, we find that old centrosomes have a higher microtubule nucleation capacity. We postulate that centrosome age breaks spindle size symmetry via microtubule nucleation even in cells thought to divide symmetrically.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":7.4,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11252449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141620073","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

Excessive STAU1 condensate drives mTOR translation and autophagy dysfunction in neurodegeneration. 在神经退行性病变中，过多的 STAU1 冷凝物会驱动 mTOR 翻译和自噬功能障碍。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2024-08-05 Epub Date: 2024-06-24 DOI: 10.1083/jcb.202311127

Ruiqian Zhao, Shijing Huang, Jingyu Li, Aihong Gu, Minjie Fu, Wei Hua, Ying Mao, Qun-Ying Lei, Boxun Lu, Wenyu Wen

{"title":"Excessive STAU1 condensate drives mTOR translation and autophagy dysfunction in neurodegeneration.","authors":"Ruiqian Zhao, Shijing Huang, Jingyu Li, Aihong Gu, Minjie Fu, Wei Hua, Ying Mao, Qun-Ying Lei, Boxun Lu, Wenyu Wen","doi":"10.1083/jcb.202311127","DOIUrl":"10.1083/jcb.202311127","url":null,"abstract":"The double-stranded RNA-binding protein Staufen1 (STAU1) regulates a variety of physiological and pathological events via mediating RNA metabolism. STAU1 overabundance was observed in tissues from mouse models and fibroblasts from patients with neurodegenerative diseases, accompanied by enhanced mTOR signaling and impaired autophagic flux, while the underlying mechanism remains elusive. Here, we find that endogenous STAU1 forms dynamic cytoplasmic condensate in normal and tumor cell lines, as well as in mouse Huntington's disease knockin striatal cells. STAU1 condensate recruits target mRNA MTOR at its 5'UTR and promotes its translation both in vitro and in vivo, and thus enhanced formation of STAU1 condensate leads to mTOR hyperactivation and autophagy-lysosome dysfunction. Interference of STAU1 condensate normalizes mTOR levels, ameliorates autophagy-lysosome function, and reduces aggregation of pathological proteins in cellular models of neurodegenerative diseases. These findings highlight the importance of balanced phase separation in physiological processes, suggesting that modulating STAU1 condensate may be a strategy to mitigate the progression of neurodegenerative diseases with STAU1 overabundance.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":7.4,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11194678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141442741","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

Binucleated human hepatocytes arise through late cytokinetic regression during endomitosis M phase. 双核人肝细胞是在内膜增生 M 期通过晚期细胞增生退化产生的。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2024-08-05 Epub Date: 2024-05-10 DOI: 10.1083/jcb.202403020

Gabriella S Darmasaputra, Cindy C Geerlings, Susana M Chuva de Sousa Lopes, Hans Clevers, Matilde Galli

{"title":"Binucleated human hepatocytes arise through late cytokinetic regression during endomitosis M phase.","authors":"Gabriella S Darmasaputra, Cindy C Geerlings, Susana M Chuva de Sousa Lopes, Hans Clevers, Matilde Galli","doi":"10.1083/jcb.202403020","DOIUrl":"10.1083/jcb.202403020","url":null,"abstract":"Binucleated polyploid cells are common in many animal tissues, where they arise by endomitosis, a non-canonical cell cycle in which cells enter M phase but do not undergo cytokinesis. Different steps of cytokinesis have been shown to be inhibited during endomitosis M phase in rodents, but it is currently unknown how human cells undergo endomitosis. In this study, we use fetal-derived human hepatocyte organoids (Hep-Orgs) to investigate how human hepatocytes initiate and execute endomitosis. We find that cells in endomitosis M phase have normal mitotic timings, but lose membrane anchorage to the midbody during cytokinesis, which is associated with the loss of four cortical anchoring proteins, RacGAP1, Anillin, SEPT9, and citron kinase (CIT-K). Moreover, reduction of WNT activity increases the percentage of binucleated cells in Hep-Orgs, an effect that is dependent on the atypical E2F proteins, E2F7 and E2F8. Together, we have elucidated how hepatocytes undergo endomitosis in human Hep-Orgs, providing new insights into the mechanisms of endomitosis in mammals.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":7.8,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11090133/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140898469","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

Regulation of cell function and identity by cellular senescence. 细胞衰老对细胞功能和特性的调节。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2024-08-05 Epub Date: 2024-06-12 DOI: 10.1083/jcb.202401112

Anda Huna, Amélie Massemin, Gabriela Makulyte, Jean-Michel Flaman, Nadine Martin, David Bernard

引用次数: 0

Proteasome gene expression is controlled by coordinated functions of multiple transcription factors. 蛋白酶体基因的表达受多种转录因子协调功能的控制。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2024-08-05 Epub Date: 2024-05-20 DOI: 10.1083/jcb.202402046

Jennifer E Gilda, Asrafun Nahar, Dharanibalan Kasiviswanathan, Nadav Tropp, Tamar Gilinski, Tamar Lahav, Dina Alexandrovich, Yael Mandel-Gutfreund, Soyeon Park, Shenhav Shemer

{"title":"Proteasome gene expression is controlled by coordinated functions of multiple transcription factors.","authors":"Jennifer E Gilda, Asrafun Nahar, Dharanibalan Kasiviswanathan, Nadav Tropp, Tamar Gilinski, Tamar Lahav, Dina Alexandrovich, Yael Mandel-Gutfreund, Soyeon Park, Shenhav Shemer","doi":"10.1083/jcb.202402046","DOIUrl":"10.1083/jcb.202402046","url":null,"abstract":"Proteasome activity is crucial for cellular integrity, but how tissues adjust proteasome content in response to catabolic stimuli is uncertain. Here, we demonstrate that transcriptional coordination by multiple transcription factors is required to increase proteasome content and activate proteolysis in catabolic states. Using denervated mouse muscle as a model system for accelerated proteolysis in vivo, we reveal that a two-phase transcriptional program activates genes encoding proteasome subunits and assembly chaperones to boost an increase in proteasome content. Initially, gene induction is necessary to maintain basal proteasome levels, and in a more delayed phase (7-10 days after denervation), it stimulates proteasome assembly to meet cellular demand for excessive proteolysis. Intriguingly, the transcription factors PAX4 and α-PALNRF-1 control the expression of proteasome among other genes in a combinatorial manner, driving cellular adaptation to muscle denervation. Consequently, PAX4 and α-PALNRF-1 represent new therapeutic targets to inhibit proteolysis in catabolic diseases (e.g., type-2 diabetes, cancer).","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":7.8,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11104393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141065337","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

Dual protection by Bcp1 and Rkm1 ensures incorporation of uL14 into pre-60S ribosomal subunits. Bcp1 和 Rkm1 的双重保护确保了 uL14 与前 60S 核糖体亚基的结合。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2024-08-05 Epub Date: 2024-07-15 DOI: 10.1083/jcb.202306117

Min-Chi Yeh, Ning-Hsiang Hsu, Hao-Yu Chu, Cheng-Han Yang, Pang-Hung Hsu, Chi-Chi Chou, Jing-Ting Shie, Wei-Ming Lee, Meng-Chiao Ho, Kai-Yin Lo

{"title":"Dual protection by Bcp1 and Rkm1 ensures incorporation of uL14 into pre-60S ribosomal subunits.","authors":"Min-Chi Yeh, Ning-Hsiang Hsu, Hao-Yu Chu, Cheng-Han Yang, Pang-Hung Hsu, Chi-Chi Chou, Jing-Ting Shie, Wei-Ming Lee, Meng-Chiao Ho, Kai-Yin Lo","doi":"10.1083/jcb.202306117","DOIUrl":"10.1083/jcb.202306117","url":null,"abstract":"Eukaryotic ribosomal proteins contain extended regions essential for translation coordination. Dedicated chaperones stabilize the associated ribosomal proteins. We identified Bcp1 as the chaperone of uL14 in Saccharomyces cerevisiae. Rkm1, the lysine methyltransferase of uL14, forms a ternary complex with Bcp1 and uL14 to protect uL14. Rkm1 is transported with uL14 by importins to the nucleus, and Bcp1 disassembles Rkm1 and importin from uL14 simultaneously in a RanGTP-independent manner. Molecular docking, guided by crosslinking mass spectrometry and validated by a low-resolution cryo-EM map, reveals the correlation between Bcp1, Rkm1, and uL14, demonstrating the protection model. In addition, the ternary complex also serves as a surveillance point, whereas incorrect uL14 is retained on Rkm1 and prevented from loading to the pre-60S ribosomal subunits. This study reveals the molecular mechanism of how uL14 is protected and quality checked by serial steps to ensure its safe delivery from the cytoplasm until its incorporation into the 60S ribosomal subunit.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":7.4,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11248248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141616497","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

Tailored assemblies of COPII proteins in secretion. 分泌过程中 COPII 蛋白的定制组装。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2024-08-05 Epub Date: 2024-07-03 DOI: 10.1083/jcb.202404013

Vivek Malhotra

引用次数: 0