Journal of Cell Biology最新文献_第9页

Mitotic genome folding. 有丝分裂基因组折叠。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-07-07 Epub Date: 2025-06-10 DOI: 10.1083/jcb.202504075

Tatsuya Hirano

引用次数: 0

Calpains orchestrate secretion of annexin-containing microvesicles during membrane repair. 钙蛋白酶在膜修复过程中协调含膜联蛋白的微泡的分泌。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-07-07 Epub Date: 2025-05-16 DOI: 10.1083/jcb.202408159

Justin Krish Williams, Jordan Matthew Ngo, Abinayaa Murugupandiyan, Dorothy E Croall, H Criss Hartzell, Randy Schekman

{"title":"Calpains orchestrate secretion of annexin-containing microvesicles during membrane repair.","authors":"Justin Krish Williams, Jordan Matthew Ngo, Abinayaa Murugupandiyan, Dorothy E Croall, H Criss Hartzell, Randy Schekman","doi":"10.1083/jcb.202408159","DOIUrl":"10.1083/jcb.202408159","url":null,"abstract":"Microvesicles (MVs) are membrane-enclosed, plasma membrane-derived particles released by cells from all branches of life. MVs have utility as disease biomarkers and may participate in intercellular communication; however, physiological processes that induce their secretion are not known. Here, we isolate and characterize annexin-containing MVs and show that these vesicles are secreted in response to the calcium influx caused by membrane damage. The annexins in these vesicles are cleaved by calpains. After plasma membrane injury, cytoplasmic calcium-bound annexins are rapidly recruited to the plasma membrane and form a scab-like structure at the lesion. In a second phase, recruited annexins are cleaved by calpains-1/2, disabling membrane scabbing. Cleavage promotes annexin secretion within MVs. Our data support a new model of plasma membrane repair, where calpains relax annexin-membrane aggregates in the lesion repair scab, allowing secretion of damaged membrane and annexins as MVs. We anticipate that cells experiencing plasma membrane damage, including muscle and metastatic cancer cells, secrete these MVs at elevated levels.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 7","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12083247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078249","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

MTMR regulates KRAS function by controlling plasma membrane levels of phospholipids. MTMR通过控制质膜磷脂水平调节KRAS功能。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-07-07 Epub Date: 2025-05-02 DOI: 10.1083/jcb.202403126

Taylor E Lange, Ali Naji, Ransome van der Hoeven, Hong Liang, Yong Zhou, Gerald R V Hammond, John F Hancock, Kwang-Jin Cho

{"title":"MTMR regulates KRAS function by controlling plasma membrane levels of phospholipids.","authors":"Taylor E Lange, Ali Naji, Ransome van der Hoeven, Hong Liang, Yong Zhou, Gerald R V Hammond, John F Hancock, Kwang-Jin Cho","doi":"10.1083/jcb.202403126","DOIUrl":"10.1083/jcb.202403126","url":null,"abstract":"KRAS, a small GTPase involved in cell proliferation and differentiation, frequently gains activating mutations in human cancers. For KRAS to function, it must bind the plasma membrane (PM) via interactions between its membrane anchor and phosphatidylserine (PtdSer). Therefore, depleting PM PtdSer abrogates KRAS PM binding and activity. From a genome-wide siRNA screen to identify genes regulating KRAS PM localization, we identified a set of phosphatidylinositol (PI) 3-phosphatases: myotubularin-related proteins (MTMR) 2, 3, 4, and 7. Here, we show that silencing MTMR 2/3/4/7 disrupts KRAS PM interactions by reducing PM PI 4-phosphate (PI4P) levels, thereby disrupting the localization and operation of ORP5, a lipid transfer protein maintaining PM PtdSer enrichment. Concomitantly, silencing MTMR 2/3/4/7 elevates PM PI3P levels while reducing PM and total PtdSer levels. We also observed MTMR 2/3/4/7 expression is interdependent. We propose that the PI 3-phosphatase activity of MTMR is required for generating PM PI, necessary for PM PI4P synthesis, promoting the PM localization of PtdSer and KRAS.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 7","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12047185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998594","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

Cargo adaptors use a handhold mechanism to engage with myosin V for organelle transport. 货物适配器使用手持机制与肌凝蛋白V进行细胞器运输。

IF 6.4 1区生物学

Journal of Cell Biology Pub Date : 2025-07-07 Epub Date: 2025-05-16 DOI: 10.1083/jcb.202408006

Hye Jee Hahn, Natalya Pashkova, Michael A Cianfrocco, Lois S Weisman

引用次数: 0

ALDH9A1 deficiency as a source of endogenous DNA damage that requires repair by the Fanconi anemia pathway. ALDH9A1缺乏作为内源性DNA损伤的来源，需要通过范可尼贫血途径修复。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-07-07 Epub Date: 2025-06-20 DOI: 10.1083/jcb.202407141

Moonjung Jung, Jungwoo Kim, Yeji Park, Isaac Ilyashov, Fan Yang, Haruna B Choijilsuren, Danielle Keahi, Jordan A Durmaz, Habin Bea, Audrey M Goldfarb, Mia D Stein, Claudia Wong, Ryan R White, Sunandini Sridhar, Raymond Noonan, Tom F Wiley, Thomas S Carroll, Francis P Lach, Sangmoo Jeong, Ileana C Miranda, Agata Smogorzewska

{"title":"ALDH9A1 deficiency as a source of endogenous DNA damage that requires repair by the Fanconi anemia pathway.","authors":"Moonjung Jung, Jungwoo Kim, Yeji Park, Isaac Ilyashov, Fan Yang, Haruna B Choijilsuren, Danielle Keahi, Jordan A Durmaz, Habin Bea, Audrey M Goldfarb, Mia D Stein, Claudia Wong, Ryan R White, Sunandini Sridhar, Raymond Noonan, Tom F Wiley, Thomas S Carroll, Francis P Lach, Sangmoo Jeong, Ileana C Miranda, Agata Smogorzewska","doi":"10.1083/jcb.202407141","DOIUrl":"10.1083/jcb.202407141","url":null,"abstract":"The Fanconi anemia (FA) DNA repair pathway is required for the repair of DNA interstrand cross-links (ICLs). ICLs are caused by genotoxins, such as chemotherapeutic agents or reactive aldehydes. Inappropriately repaired ICLs contribute to hematopoietic stem cell (HSC) failure and tumorigenesis. While endogenous acetaldehyde and formaldehyde are known to induce HSC failure and leukemia in FA patients, the effects of other toxic metabolites on FA pathogenesis have not been systematically investigated. Using a metabolism-focused CRISPR screen, we found a synthetically lethal interaction between ALDH9A1 and the deficiency of the FA pathway. Combined deficiency of ALDH9A1 and FANCD2 causes genomic instability, apoptosis, and decreased hematopoietic colony formation. Fanca-/-Aldh9a1-/- mice exhibited an increased incidence of ovarian tumors. A suppressor CRISPR screen revealed that the loss of ATP13A3, a polyamine transporter, resulted in improved survival of FANCD2-/-ALDH9A1-/- cells. These findings nominate high intracellular polyamines and the resulting 3-aminopropanal and acrolein as sources of endogenous DNA damage in patients with FA.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 7","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12187107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333223","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

Sphingolipid synthesis maintains nuclear membrane integrity and genome stability during cell division. 鞘脂合成在细胞分裂过程中维持核膜的完整性和基因组的稳定性。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-07-03 DOI: 10.1083/jcb.202407209

Sunyoung Hwang,William Russo,Jaylah Cormier,Jillian Johnson,Sara Martin,Marica Rosaria Ippolito,Sara Cordone,Rui Li,Lihua Julie Zhu,Stefano Santaguida,Eduardo M Torres

{"title":"Sphingolipid synthesis maintains nuclear membrane integrity and genome stability during cell division.","authors":"Sunyoung Hwang,William Russo,Jaylah Cormier,Jillian Johnson,Sara Martin,Marica Rosaria Ippolito,Sara Cordone,Rui Li,Lihua Julie Zhu,Stefano Santaguida,Eduardo M Torres","doi":"10.1083/jcb.202407209","DOIUrl":"https://doi.org/10.1083/jcb.202407209","url":null,"abstract":"Lipid synthesis must be precisely regulated to support membrane growth and organelle biogenesis during cell division, yet little is known about how this process is coordinated with other cell cycle events. Here, we show that de novo synthesis of sphingolipids during the S and G2 phases of the cell cycle is essential to increasing nuclear membranes. Indeed, the products of serine palmitoyltransferase (SPT), long-chain bases, localize to the nucleus and are integral components of nuclear membranes in yeast and human cells. Importantly, inhibition of SPT fails to induce cell cycle arrest, causing nuclear membrane collapse and loss of viability in yeast cells. In human cells, this causes abnormal nuclear morphology and genomic instability, evidenced by the increased incidence of nuclear blebs, micronuclei, anaphase bridges, and multipolar mitosis. These results indicate that dysregulated cell division under low sphingolipid availability can drive several disease-associated phenotypes, including aberrant nuclear morphologies and genomic instability.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"26 1","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144547880","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

Delta tubulin stabilizes male meiotic kinetochores and aids microtubule remodeling and fertility. 微管蛋白稳定雄性减数分裂着丝点，帮助微管重塑和生育。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-06-30 DOI: 10.1083/jcb.202412056

G Gemma Stathatos,D Jo Merriner,Anne E O'Connor,Jennifer Zenker,Jessica E M Dunleavy,Moira K O'Bryan

{"title":"Delta tubulin stabilizes male meiotic kinetochores and aids microtubule remodeling and fertility.","authors":"G Gemma Stathatos,D Jo Merriner,Anne E O'Connor,Jennifer Zenker,Jessica E M Dunleavy,Moira K O'Bryan","doi":"10.1083/jcb.202412056","DOIUrl":"https://doi.org/10.1083/jcb.202412056","url":null,"abstract":"Delta tubulin (TUBD1) is a noncanonical tubulin protein that has been linked to complex microtubule structures in somatic cell lines and unicellular species. Its role in mammals remains enigmatic; however, TUBD1 is enriched within mammalian male germ cells. Herein, we have defined new roles for TUBD1 during male germ cell development in vivo using a conditional knockout mouse model and shown that spermatogenesis in the absence of TUBD1 causes sterility. We show TUBD1 stabilizes kinetochores during male mouse meiosis, enabling meiotic progression, and that it is required for appropriate spindle polarity and cytokinesis. Subsequently, in haploid cells, TUBD1 works in partnership with the microtubule-severing enzymes KATNAL2 and KATNB1 to regulate manchette remodeling and shape the sperm head. Collectively, these findings reveal TUBD1 plays a key role in the formation and function of highly specialized microtubule structures in mammalian spermatogenesis. Advanced knowledge of TUBD1 may generate new insights into underlying causes of diseases associated with infertility or development.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"8 1","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144521463","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

The PAX3-FOXO1 fusion gene reduces cell-ECM interactions and TGFβ signaling in rhabdomyosarcoma. PAX3-FOXO1融合基因减少横纹肌肉瘤中细胞- ecm相互作用和TGFβ信号传导。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-06-30 DOI: 10.1083/jcb.202408155

Antonios Chronopoulos,Ivan Chavez,Chandra Kaladhar Vemula,Nikhil Mittal,Vic Zamloot,Yuanzhong Pan,Sangyoon J Han,JinSeok Park

引用次数: 0

PLK-1 suppresses centrosome maturation and microtubule polymerization to ensure faithful oocyte meiosis. PLK-1抑制中心体成熟和微管聚合以确保卵母细胞忠实减数分裂。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-06-27 DOI: 10.1083/jcb.202503080

Juhi G Narula,Sarah M Wignall

{"title":"PLK-1 suppresses centrosome maturation and microtubule polymerization to ensure faithful oocyte meiosis.","authors":"Juhi G Narula,Sarah M Wignall","doi":"10.1083/jcb.202503080","DOIUrl":"https://doi.org/10.1083/jcb.202503080","url":null,"abstract":"Sexual reproduction relies on meiosis, a specialized cell division program that produces haploid gametes. Oocytes of most organisms lack centrosomes, and therefore chromosome segregation is mediated by acentrosomal spindles. Here, we explore the role of Polo-like kinase 1 (PLK-1) in Caenorhabditiselegans oocytes, revealing mechanisms that ensure the fidelity of this unique form of cell division. Previously, PLK-1 was shown to be required for nuclear envelope breakdown and chromosome segregation in oocytes. We now find that PLK-1 is also required for establishing and maintaining acentrosomal spindle organization and for preventing excess microtubule polymerization in these cells. Additionally, our studies revealed an unexpected new role for this essential kinase. While PLK-1 is known to be required for centrosome maturation during mitosis, we found that either removal of PLK-1 from oocytes or inhibition of its kinase activity caused premature recruitment of pericentriolar material to the sperm-provided centrioles following fertilization. Thus, PLK-1 suppresses centrosome maturation during oocyte meiosis, which is opposite to its role in mitosis. Taken together, our work identifies PLK-1 as a key player that promotes faithful acentrosomal meiosis in oocytes and demonstrates that its catalytic activity is required for carrying out these important roles.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"18 1","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504631","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

Dynamic interaction of spliceosomal snRNPs with coilin explains Cajal body characteristics. 剪接体snRNPs与卷曲蛋白的动态相互作用解释了Cajal体特征。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-06-25 DOI: 10.1083/jcb.202309128

Davide A Basello,Michaela Blažíková,Adriana Roithová,Martina Hálová,Nenad Radivojević,Karla M Neugebauer,David Staněk

引用次数: 0