Journal of cell science最新文献_第2页

ATP synthase epsilon subunit: An unconventional adaptor of clathrin-mediated endocytosis of hemoglobin in Leishmania. ATP合成酶epsilon亚基：利什曼原虫中网格蛋白介导的血红蛋白内吞作用的非常规适配器。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-06-18 DOI: 10.1242/jcs.263555

Anjali Kapoor, Jitender Kumar Verma, Deepali Goyal, Shruti Agarwal, Aditi Gaur, Amitabha Mukhopadhyay

{"title":"ATP synthase epsilon subunit: An unconventional adaptor of clathrin-mediated endocytosis of hemoglobin in Leishmania.","authors":"Anjali Kapoor, Jitender Kumar Verma, Deepali Goyal, Shruti Agarwal, Aditi Gaur, Amitabha Mukhopadhyay","doi":"10.1242/jcs.263555","DOIUrl":"https://doi.org/10.1242/jcs.263555","url":null,"abstract":"In clathrin-mediated endocytosis, cytoplasmic domain of the receptor binds with AP2-adaptor which recruits clathrin to mediate endocytosis. Classical AP2-adaptor Leishmania is not yet characterized. Here, we have identified ATP Synthase epsilon (LdATPSɛ) subunit as a novel adaptor in Leishmania using yeast two-hybrid screening. Subsequently, we have cloned and expressed LdATPSɛ from Leishmania and have shown that LdATPSɛ co-localizes with LdClathrin and hemoglobin receptor in Leishmania. We have found that LdATPSɛ directly binds with cargo-binding motif 'YLAP' in the cytoplasmic domain of LdHbR, whereas it interacts with LdClathrin terminal domain via clathrin-binding motif 'LSELD'. Consequently, we have shown that mutated clathrin-binding box LdATPSɛL133A/L136A/D137A does not bind with clathrin, fails to localize in the flagellar pocket and its overexpression completely blocks the hemoglobin internalization in Leishmania. LdATPSɛ-/- knock out parasites are not viable indicating its essential function. However, hemoglobin internalization in LdATPSɛ+/- parasites is significantly blocked and LdATPSɛ+/- parasites fails to grow in macrophages as parasite in unable internalize hemoglobin. Our results have demonstrated that LdATPSɛ is a novel adaptor for clathrin in hemoglobin endocytosis in Leishmania.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144484529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Differential roles of cyclin-CDK1 complexes in cell migration and invasion. 细胞周期蛋白- cdk1复合物在细胞迁移和侵袭中的不同作用。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-06-16 DOI: 10.1242/jcs.263697

Joseph H R Hetmanski, Michael J Jones, Matthew Hartshorn, Patrick T Caswell, Matthew C Jones

引用次数: 0

Conserved biochemical activity and function of phosphatidylinositol 5 phosphate 4 kinase regulates growth & development. 磷脂酰肌醇5磷酸4激酶的保守生化活性和功能调控着生长发育。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-06-16 DOI: 10.1242/jcs.263881

Harini Krishnan, Suhail Muzaffar, Sanjeev Sharma, Visvanathan Ramya, Avishek Ghosh, Ramanathan Sowdhamini, Raghu Padinjat

{"title":"Conserved biochemical activity and function of phosphatidylinositol 5 phosphate 4 kinase regulates growth & development.","authors":"Harini Krishnan, Suhail Muzaffar, Sanjeev Sharma, Visvanathan Ramya, Avishek Ghosh, Ramanathan Sowdhamini, Raghu Padinjat","doi":"10.1242/jcs.263881","DOIUrl":"10.1242/jcs.263881","url":null,"abstract":"Co-ordination of function between multiple cells, mediated by hormones or growth factors, is a critical requirement for multi-cellularity. Phosphoinositides, generated by lipid kinase activity, are second messengers that mediate such signalling. Phosphatidylinositol 5 phosphate 4-kinase (PIP4K) is a lipid kinase that phosphorylates phosphatidylinositol 5-phosphate (PI5P) to generate phosphatidylinositol 4,5 bisphosphate [PI(4,5)P2]. A comprehensive bioinformatics analysis of the tree of life, revealed that PIP4K is a metazoan-specific enzyme, but with homologs in choanoflagellates. We find that PIP4K from the sponge Amphimedon queenslandica (AqPIP4K), regarded as the earliest evolved metazoan, shows biochemical activity highly conserved with human PIP4K. Further, AqPIP4K was able to rescue the reduced cell size, growth and development of a Drosophila PIP4K mutant. These phenotypes are regulated through activity of the insulin receptor, a member of the receptor tyrosine kinase family, that is unique to metazoans. Overall, our work defines PIP4K as part of a signal transduction motif required to regulate receptor tyrosine kinase signalling for intercellular communication in the earliest forms of metazoans.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

A data-driven model for mitochondrial inner membrane remodeling as a driving force of organelle shaping. 线粒体内膜重塑作为细胞器形成驱动力的数据驱动模型。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-06-15 Epub Date: 2025-06-20 DOI: 10.1242/jcs.263850

Noga Preminger, Ben Zucker, Sarah Hassdenteufel, Till Stephan, Stefan Jakobs, Michael M Kozlov, Maya Schuldiner

{"title":"A data-driven model for mitochondrial inner membrane remodeling as a driving force of organelle shaping.","authors":"Noga Preminger, Ben Zucker, Sarah Hassdenteufel, Till Stephan, Stefan Jakobs, Michael M Kozlov, Maya Schuldiner","doi":"10.1242/jcs.263850","DOIUrl":"10.1242/jcs.263850","url":null,"abstract":"Mitochondria are dynamic organelles exhibiting diverse shapes. Although variation in mitochondrial shapes, which range from spheres to elongated tubules, and the transitions between them are clearly seen in many cell types, the molecular mechanisms governing this morphological variability remain poorly understood. Here, we propose a biophysical model for the shape transition between spheres and tubules based on the interplay between the inner and outer mitochondrial membranes. Our model suggests that the difference in surface area, arising from folding of the inner membrane into cristae, correlates with mitochondrial elongation. Analysis of live-cell super-resolution microscopy data supports this correlation, linking elongated shapes to the extent of cristae in the inner membrane. Knocking down cristae-shaping proteins further confirms the impact on mitochondrial shape, demonstrating that defects in cristae formation correlate with mitochondrial sphericity. Our results suggest that the dynamics of the inner mitochondrial membrane are not only important for simply creating surface area required for respiratory capacity but go beyond that to affect the whole organelle morphology. This work explores the biophysical foundations that govern the shape of individual mitochondria, suggesting potential links between mitochondrial structure and function. This should be of profound significance, particularly in the context of disrupted cristae-shaping proteins and their implications in mitochondrial diseases.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

SLC-25A46 regulates mitochondrial fusion through the mitofusin protein FZO-1 and is essential for maintaining neuronal morphology. SLC-25A46通过FZO-1/Mitofusin调控线粒体融合。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-06-15 Epub Date: 2025-06-23 DOI: 10.1242/jcs.263571

Hiroyuki Obinata, Taisei Watanabe, Hironori Takahashi, Satoshi Shimo, Toshiyuki Oda, Asako Sugimoto, Shinsuke Niwa

{"title":"SLC-25A46 regulates mitochondrial fusion through the mitofusin protein FZO-1 and is essential for maintaining neuronal morphology.","authors":"Hiroyuki Obinata, Taisei Watanabe, Hironori Takahashi, Satoshi Shimo, Toshiyuki Oda, Asako Sugimoto, Shinsuke Niwa","doi":"10.1242/jcs.263571","DOIUrl":"10.1242/jcs.263571","url":null,"abstract":"Mitochondria are dynamic organelles shaped by sequential fission and fusion events. The mitochondrial protein SLC25A46 has been identified as a causative gene for mitochondrial neuropathies. However, the function of SLC25A46 in mitochondrial morphogenesis remains controversial, with several reports suggesting it acts as a mitochondrial fission factor, whereas others propose it as a fusion factor. In this study, employing forward genetics, we identified slc-25A46, a Caenorhabditis elegans ortholog of human SLC25A46, as an essential factor for mitochondrial fusion. Suppressor mutagenesis screening revealed loss-of-function mutations in drp-1, a mitochondrial fission factor, as suppressors of slc-25A46. The phenotype of slc-25A46 mutants is similar to that of mutants in the worm mitofusin ortholog fzo-1, wherein the mitochondrial fusion factor is disrupted. Overexpressing FZO-1 mitigated mitochondrial defects in slc-25a46 mutants, indicating that SLC-25A46 promotes fusion through FZO-1. Disease model worms carrying mutations associated with SLC25A46 exhibited mitochondrial fragmentation and accelerated neurodegeneration, suggesting that slc-25A46 maintains neuronal morphology through regulating mitochondrial fusion regulation.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

In vitro reconstitution of a minimal human centrosome scaffold capable of forming and clustering microtubule asters. 能够形成和聚集微管紫菀的最小人类中心体支架的体外重建。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-06-15 Epub Date: 2025-06-27 DOI: 10.1242/jcs.264121

Manolo U Rios, Weronika E Stachera, Nicole E Familiari, Claudia Brito, Thomas Surrey, Jeffrey B Woodruff

{"title":"In vitro reconstitution of a minimal human centrosome scaffold capable of forming and clustering microtubule asters.","authors":"Manolo U Rios, Weronika E Stachera, Nicole E Familiari, Claudia Brito, Thomas Surrey, Jeffrey B Woodruff","doi":"10.1242/jcs.264121","DOIUrl":"10.1242/jcs.264121","url":null,"abstract":"CDK5RAP2 (also known as CEP215) is a key pericentriolar material (PCM) protein that recruits microtubule-nucleating factors at human centrosomes. Here, using an in vitro reconstitution system, we show that CDK5RAP2 is sufficient to form micron-scale scaffolds using nanometer-scale nucleators in a PLK-1-regulated manner. CDK5RAP2 assemblies recruited and activated γ-tubulin ring complexes (γ-TuRCs) which, in the presence of α/β-tubulin, generated microtubule asters. We found that amino acid F75 in CDK5RAP2 helps to recruit γ-TuRC and is indispensable for γ-TuRC activation. Furthermore, our system recapitulated key features of centrosome-amplified cancer cells. CDK5RAP2 scaffolds recruited the molecular motor HSET (also known as KifC1), which enhanced concentration of α/β-tubulin, microtubule polymerization and clustering of the assemblies. Our results highlight the specificity and selectivity of in vitro-generated CDK5RAP2 scaffolds, and identify a minimal set of components required for human PCM assembly and function. This minimal model offers a powerful tool for studying centrosome biology and dysfunction in human health and disease.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

A role for class I p21-activated kinases in the regulation of the excitability of the actin cytoskeleton. 一类p21活化激酶在肌动蛋白细胞骨架兴奋性调控中的作用。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-06-15 Epub Date: 2025-06-23 DOI: 10.1242/jcs.263763

Joe J Tyler, Anthony Davidson, Megan E Poxon, Montserrat Llanses Martinez, Pete Hume, Jason S King, Vassilis Koronakis

{"title":"A role for class I p21-activated kinases in the regulation of the excitability of the actin cytoskeleton.","authors":"Joe J Tyler, Anthony Davidson, Megan E Poxon, Montserrat Llanses Martinez, Pete Hume, Jason S King, Vassilis Koronakis","doi":"10.1242/jcs.263763","DOIUrl":"10.1242/jcs.263763","url":null,"abstract":"The p21-activated kinases (PAKs) are involved in a range of functions, including the regulation of the actin cytoskeleton. However, although many PAK substrates identified have been implicated in the regulation of the actin cytoskeleton, a coherent picture of the total effect of PAK activation on the state of the actin cytoskeleton is unclear. Here, we show that, in mouse embryonic fibroblasts, inhibition of class I PAK kinase activity by small-molecule inhibitors leads to the constitutive production of the phosphoinositide phosphatidylinositol (3,4,5)-trisphosphate [PI(3,4,5)P3] on the ventral surface of the cell. The formation of patches of PI(3,4,5)P3 remodels the actin cytoskeleton and polarises the cell. From the overexpression of truncated and mutated PAK1 and PAK2 constructs, as well as an in vitro model of PAK activation, we propose that this is driven by a hyper recruitment of class I PAK and PAK-binding partners. This aberrant production of PI(3,4,5)P3 suggests that, by limiting its own recruitment, the kinase activity of class I PAKs acts to downregulate phosphoinositide 3-kinase (PI3K) activity, further highlighting class I PAKs as regulators of PI3K activity and therefore the excitability of the actin cytoskeleton.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":"138 12","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

A cryo-electron microscopy structure of yeast Pex5 in complex with a cargo uncovers a novel binding interface. 酵母Pex5与货物复合物的低温电镜结构揭示了一个新的结合界面。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-06-15 Epub Date: 2025-06-26 DOI: 10.1242/jcs.263890

Lior Peer, Orly Dym, Nadav Elad, Asa Tirosh, Jossef Jacobovitch, Ehud Sivan, Mor Angel, Shira Albeck, Maya Schuldiner, Yoav Peleg, Einat Zalckvar

{"title":"A cryo-electron microscopy structure of yeast Pex5 in complex with a cargo uncovers a novel binding interface.","authors":"Lior Peer, Orly Dym, Nadav Elad, Asa Tirosh, Jossef Jacobovitch, Ehud Sivan, Mor Angel, Shira Albeck, Maya Schuldiner, Yoav Peleg, Einat Zalckvar","doi":"10.1242/jcs.263890","DOIUrl":"10.1242/jcs.263890","url":null,"abstract":"Proper protein targeting to organelles is crucial for maintaining eukaryotic cellular function and homeostasis. This necessity has driven the evolution of specific targeting signals on proteins and the targeting factors that recognize them. A prominent example is peroxisomal matrix proteins, most of which depend on the targeting factor Pex5 to localize and function correctly. Although most Pex5 cargoes contain a peroxisomal targeting signal type 1 (PTS1), they are not all targeted similarly. Some undergo priority targeting, facilitated either by stronger binding to specific subsets of PTS1 signals or by additional interaction interfaces. These observations highlight the extensive complexity of Pex5-mediated targeting. In this study, we reveal that the Saccharomyces cerevisiae (yeast) matrix protein Eci1 can reach peroxisomes and bind Pex5 in the absence of PTS1. By solving the structure of the yeast Pex5-Eci1 complex using cryo-electron microscopy, we identified additional binding interfaces. Our findings provide new insights into the versatile interactions between Pex5 and its cargo, Eci1. More broadly, this work highlights the intricate, dynamic nature of the interactions between cargo factors and their cargoes to meet the complex environment within eukaryotic cells.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Endosomal RFFL ubiquitin ligase regulates mitochondrial morphology by targeting mitofusin 2. 内体RFFL泛素连接酶通过靶向Mitofusin 2调控线粒体形态。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-06-15 Epub Date: 2025-06-20 DOI: 10.1242/jcs.263830

Nikhil Dev Narendradev, Rishith Ravindran, Parul Jain, Shikha Chaudhary, Anoop Kumar G Velikkakath, Abyasree Sudharman, Adithya Janardhanan, Tapas Chandra Nag, Subhash Chandra Yadav, Srinivasa Murty Srinivasula

{"title":"Endosomal RFFL ubiquitin ligase regulates mitochondrial morphology by targeting mitofusin 2.","authors":"Nikhil Dev Narendradev, Rishith Ravindran, Parul Jain, Shikha Chaudhary, Anoop Kumar G Velikkakath, Abyasree Sudharman, Adithya Janardhanan, Tapas Chandra Nag, Subhash Chandra Yadav, Srinivasa Murty Srinivasula","doi":"10.1242/jcs.263830","DOIUrl":"10.1242/jcs.263830","url":null,"abstract":"Mitochondrial homeostasis is ensured through communication between diverse cellular organelles, including mitochondria, the endoplasmic reticulum (ER), lysosomes and endosomes. Although it is known that mitofusins regulate mitochondrial networks and ER contacts, their role in endosomal-mitochondrial interactions remains unclear. Previously, we have reported that vesicles positive for the endosomal ubiquitin ligase RFFL are associated with damaged mitochondria and prime the organelle for PRKN recruitment. Now, we establish that RFFL is a ubiquitin ligase for mitofusin 2 (MFN2). Using electron microscopy and confocal imaging analyses, we demonstrate that RFFL-knockout cells exhibit enlarged mitochondrial morphology. RFFL interacts at an endogenous level with MFN2 and contributes to its ubiquitylation upon mitochondrial damage. Recombinant RFFL interacts and ubiquitylates MFN2 protein in vitro. Furthermore, exogenous RFFL, in a ligase-dependent manner, specifically reduces the exogenous protein levels of both MFN1 and MFN2, but not that of DRP1, and also perturbs lipid homeostasis. Importantly, we show that the hyperfused mitochondria morphology reported with expression of pathogenic disease mutants of MFN2 (T206I and R364W) of Charcot-Marie-Tooth disease type 2A can be rescued by RFFL co-expression. The study unravels novel mechanisms involving endosomal ubiquitin ligases in mitochondrial networks.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144182247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

CLASP1 regulates Dynein for PLK1-mediated spindle organization and cytokinesis in oocyte meiosis. CLASP1在卵母细胞减数分裂中调控plk1介导的纺锤体组织和细胞分裂的动力蛋白。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-06-12 DOI: 10.1242/jcs.264015

Meng-Meng Shan, Ping-Shuang Lu, Yuan-Jing Zou, Kun-Huan Zhang, Jing-Cai Liu, Jia-Qian Ju, Shao-Chen Sun

{"title":"CLASP1 regulates Dynein for PLK1-mediated spindle organization and cytokinesis in oocyte meiosis.","authors":"Meng-Meng Shan, Ping-Shuang Lu, Yuan-Jing Zou, Kun-Huan Zhang, Jing-Cai Liu, Jia-Qian Ju, Shao-Chen Sun","doi":"10.1242/jcs.264015","DOIUrl":"https://doi.org/10.1242/jcs.264015","url":null,"abstract":"The meiotic spindle organization and cytokinesis are important for mammalian oocyte maturation. CLIP-associating protein (CLASP) 1 is a member of microtubule plus-end binding proteins, which is reported to regulate cytokinesis in mitosis; however, the functions of CLASP1 in meiosis are still unclear. In this study, we reported that CLASP1 played critical roles both at metaphase and telophase in mouse oocyte meiosis. Our results indicated that CLASP1 was essential for oocyte maturation and its depletion caused the spindle organization and microtubule-kinetochore attachment defects at metaphase Ⅰ, while this might be due to its association with PLK1/p-MAPK. Besides, deacetylases HDAC6/ SIRT1 were found to be decreased which further affected tubulin acetylation level and microtubule stability after CLASP1 depletion. We also showed that CLASP1 could associate with PLK1/PRC1-based central spindle formation and cytokinesis at telophase Ⅰ. Moreover, Dynein was recognized to interact closely with CLASP1 and may function as a downstream motor protein involved in the orderly transport of PLK1. Taken together, we demonstrated that CLASP1 may play multiple roles in Dynein-based PLK1 for spindle organization and cytokinesis in mouse oocyte meiosis.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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