Journal of Cell Biology最新文献

Nonmuscle myosin II regulates presynaptic actin and neuronal mechanobiology in Drosophila. 非肌球蛋白II调节果蝇突触前肌动蛋白和神经元力学生物学。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-09-01 Epub Date: 2025-07-11 DOI: 10.1083/jcb.202501211

Biljana Ermanoska, Jonathan Baets, Avital A Rodal

{"title":"Nonmuscle myosin II regulates presynaptic actin and neuronal mechanobiology in Drosophila.","authors":"Biljana Ermanoska, Jonathan Baets, Avital A Rodal","doi":"10.1083/jcb.202501211","DOIUrl":"https://doi.org/10.1083/jcb.202501211","url":null,"abstract":"Neuromuscular junctions (NMJs) are evolutionarily ancient, specialized contacts between neurons and muscles. They experience lifelong strain, yet the mechanism preserving their integrity under mechanical load remains unclear. Here, we identify a novel actomyosin structure at Drosophila larval NMJs, consisting of a long-lived, low-turnover presynaptic actin core that colocalizes with nonmuscle myosin II (NMII) and becomes disorganized upon manipulating neuronal NMII levels or activity. Intriguingly, neuronal NMII depletion altered postsynaptic NMII levels and organization near synapses, suggesting transsynaptic propagation of actomyosin rearrangements. Under these conditions, integrin adhesion receptors were reduced on both sides of the synapse, indicating disrupted neuron-muscle connections. Notably, axon severing mimics these effects, while axonal stretching reorganizes integrins without disrupting the actin core, suggesting that presynaptic actomyosin and integrin organization are highly sensitive to mechanical cues and dynamically adjust to both loss and gain of tension. Our study reveals a presynaptic actomyosin assembly that maintains mechanical continuity between neurons and muscle, potentially enabling mechanotransduction at the NMJ through integrin-mediated adhesion.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 9","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144612166","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

CDR2 is a dynein adaptor recruited by kinectin to regulate ER sheet organization. CDR2是由运动蛋白募集的动力蛋白适配体，调节内质网片的组织。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-09-01 Epub Date: 2025-07-10 DOI: 10.1083/jcb.202411034

Vanessa Teixeira, Kashish Singh, José B Gama, Matilde Moreira, Ricardo Celestino, Ana Xavier Carvalho, Paulo S Pereira, Carla M C Abreu, Tiago J Dantas, Andrew P Carter, Reto Gassmann

{"title":"CDR2 is a dynein adaptor recruited by kinectin to regulate ER sheet organization.","authors":"Vanessa Teixeira, Kashish Singh, José B Gama, Matilde Moreira, Ricardo Celestino, Ana Xavier Carvalho, Paulo S Pereira, Carla M C Abreu, Tiago J Dantas, Andrew P Carter, Reto Gassmann","doi":"10.1083/jcb.202411034","DOIUrl":"10.1083/jcb.202411034","url":null,"abstract":"The ER relies on the microtubule cytoskeleton for the organization of its extended membrane network, but how microtubule-based motors contribute remains unclear. Using biochemical and cell-based assays, we identify cerebellar degeneration-related protein 2 (CDR2) and its paralog CDR2-like (CDR2L), onconeural antigens with poorly understood functions, as ER adaptors for cytoplasmic dynein-1 (dynein). We demonstrate in human cancer cells that CDR2 is recruited by the integral ER membrane protein kinectin (KTN1) and that double knockout of CDR2 and CDR2L enhances KTN1-dependent ER sheet stacking, reversal of which by exogenous CDR2 requires its dynein-binding CC1 box motif. Exogenous CDR2 expression additionally promotes CC1 box-dependent clustering of ER sheets near centrosomes. CDR2 competes with the eEF1Bβ subunit of translation elongation factor 1 for binding to KTN1, and eEF1Bβ knockdown increases endogenous CDR2 levels on ER sheets, inducing their centrosome-proximal clustering. Our study describes a novel molecular pathway that implicates dynein in ER sheet organization and may be involved in the pathogenesis of paraneoplastic cerebellar degeneration.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 9","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600576","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

Nodal modulator (NOMO) is a force-bearing transmembrane protein required for muscle differentiation. Nodal modulator （NOMO）是肌肉分化所需的一种力承受力跨膜蛋白。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-09-01 Epub Date: 2025-07-15 DOI: 10.1083/jcb.202505010

Brigitte S Naughton, Swapnil C Devarkar, Vanessa Todorow, Sunanda Mallik, Stacey Oxendine, Sanjana Junnarkar, Yuan Ren, Julien Berro, Janine Kirstein, Yong Xiong, Christian Schlieker

{"title":"Nodal modulator (NOMO) is a force-bearing transmembrane protein required for muscle differentiation.","authors":"Brigitte S Naughton, Swapnil C Devarkar, Vanessa Todorow, Sunanda Mallik, Stacey Oxendine, Sanjana Junnarkar, Yuan Ren, Julien Berro, Janine Kirstein, Yong Xiong, Christian Schlieker","doi":"10.1083/jcb.202505010","DOIUrl":"https://doi.org/10.1083/jcb.202505010","url":null,"abstract":"The ER relies on membrane-shaping proteins to maintain a continuous network of sheets and tubules that host distinct biological processes. How this intricate structure of the ER membrane system is maintained under conditions of mechanical strain is incompletely understood. NOMO is an ER-resident transmembrane protein that contributes to ER morphology and is highly expressed in striated muscle. In this study, we identify a critical interface between distal Ig domains that enables NOMO to maintain ER morphology and bear mechanical forces. By incorporating two independent tension sensors in the luminal domain of NOMO, we demonstrate that NOMO assemblies experience forces in the single piconewton range, with a significant contribution from the identified interface. These newly defined features are important-if not indispensable-for myogenesis, as interface mutations affecting mechanosensitivity fail to restore the essential role of NOMO during myogenesis in a C2C12 differentiation model. Moreover, NOMO depletion impairs nematode motility, underscoring a broader functional importance in muscle physiology.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 9","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637133","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

Arc controls organ architecture through modulation of Crb and MyoII. Arc通过调节Crb和MyoII来控制器官结构。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-09-01 Epub Date: 2025-06-12 DOI: 10.1083/jcb.202409078

Ji Hoon Kim, Rika Maruyama, Kwon Kim, Devin A Vertrees, Parama Paul, Kyla Britson, Nathaniel R Laughner, Deborah J Andrew

{"title":"Arc controls organ architecture through modulation of Crb and MyoII.","authors":"Ji Hoon Kim, Rika Maruyama, Kwon Kim, Devin A Vertrees, Parama Paul, Kyla Britson, Nathaniel R Laughner, Deborah J Andrew","doi":"10.1083/jcb.202409078","DOIUrl":"10.1083/jcb.202409078","url":null,"abstract":"Precise orchestration of morphogenetic processes generates organs that are optimally positioned and the right size and shape to fit and maximize functionality. Here, we show that Arc, a large apical membrane-associated PDZ domain-containing protein, works through the apical determinant Crumbs to limit non-muscle myosin II (MyoII) activity during tissue invagination in the Drosophila salivary gland (SG). We show that loss of Arc, attenuation of Crumbs, and increased activation of MyoII leads to the simultaneous internalization of more precursor cells than normal. Consequently, mature SGs are shorter with more cells surrounding the lumen all along the tube. Correspondingly, overexpression of Arc or SG-specific knockdown of MyoII leads to longer SGs with fewer cells surrounding the lumen. Our findings support a model wherein plasma membrane (PM)-associated Crumbs stabilizes cellular junctions by limiting apical pools of activated MyoII and countering the destabilizing effects of MyoII at the PM, limiting how many cells internalize at any given time, shaping final tube geometry.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 9","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12160935/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274959","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

Visualizing nuclear pore complex plasticity with pan-expansion microscopy. 用泛膨胀显微镜观察核孔复合塑性。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-09-01 Epub Date: 2025-06-12 DOI: 10.1083/jcb.202409120

Kimberly J Morgan, Emma Carley, Alyssa N Coyne, Jeffrey D Rothstein, C Patrick Lusk, Megan C King

{"title":"Visualizing nuclear pore complex plasticity with pan-expansion microscopy.","authors":"Kimberly J Morgan, Emma Carley, Alyssa N Coyne, Jeffrey D Rothstein, C Patrick Lusk, Megan C King","doi":"10.1083/jcb.202409120","DOIUrl":"10.1083/jcb.202409120","url":null,"abstract":"The exploration of cell-type and environmentally responsive nuclear pore complex (NPC) plasticity requires new, accessible tools. Using pan-expansion microscopy (pan-ExM), NPCs were identified by machine learning-facilitated segmentation. They exhibited a large range of diameters with a bias for dilated NPCs at the basal nuclear surface in clusters suggestive of local islands of nuclear envelope tension. Whereas hyperosmotic shock constricted NPCs analogously to those found in annulate lamellae, depletion of LINC complexes specifically eliminated the modest nuclear surface diameter biases. Therefore, LINC complexes may contribute locally to nuclear envelope tension to toggle NPC diameter between dilated, but not constricted, states. Lastly, POM121 shifts from the nuclear ring to the inner ring of the NPC specifically in induced pluripotent stem cell-derived neurons from a patient with C9orf72 amyotrophic lateral sclerosis. Thus, pan-ExM is a powerful tool to visualize NPC plasticity in physiological and pathological contexts at single NPC resolution.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 9","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12162248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274960","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

Optogenetic and chemical genetic tools for rapid repositioning of vimentin intermediate filaments. 光遗传学和化学遗传学工具快速重新定位vimentin中间细丝。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-09-01 Epub Date: 2025-07-08 DOI: 10.1083/jcb.202504004

Milena Pasolli, Joyce C M Meiring, James P Conboy, Gijsje H Koenderink, Anna Akhmanova

{"title":"Optogenetic and chemical genetic tools for rapid repositioning of vimentin intermediate filaments.","authors":"Milena Pasolli, Joyce C M Meiring, James P Conboy, Gijsje H Koenderink, Anna Akhmanova","doi":"10.1083/jcb.202504004","DOIUrl":"10.1083/jcb.202504004","url":null,"abstract":"Intermediate filaments (IFs) are a key component of the cytoskeleton, essential for regulating cell mechanics, maintaining nuclear integrity, organelle positioning, and modulating cell signaling. Current insights into IF function primarily come from studies using long-term perturbations, such as protein depletion or mutation. Here, we present tools that allow rapid manipulation of vimentin IFs in the whole cytoplasm or within specific subcellular regions by inducibly coupling them to microtubule motors, either pharmacologically or using light. Rapid perinuclear clustering of vimentin had no major immediate effects on the actin or microtubule organization, cell spreading, or focal adhesion number, but it reduced cell stiffness. Mitochondria and endoplasmic reticulum (ER) sheets were reorganized due to vimentin clustering, whereas lysosomes were only briefly displaced and rapidly regained their normal distribution. Keratin moved along with vimentin in some cell lines but remained intact in others. Our tools help to study the immediate and local effects of vimentin perturbation and identify direct links of vimentin to other cellular structures.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 9","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12237251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584017","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

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 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-09-01 Epub 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":"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":"224 9","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505767","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

Structure of the microtubule-anchoring factor NEDD1 bound to the γ-tubulin ring complex. 结合γ-微管蛋白环复合物的微管锚定因子NEDD1的结构。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-08-04 Epub Date: 2025-05-21 DOI: 10.1083/jcb.202410206

Hugo Muñoz-Hernández, Yixin Xu, Aitor Pellicer Camardiel, Daniel Zhang, Allen Xue, Amol Aher, Ellie Walker, Florina Marxer, Tarun M Kapoor, Michal Wieczorek

{"title":"Structure of the microtubule-anchoring factor NEDD1 bound to the γ-tubulin ring complex.","authors":"Hugo Muñoz-Hernández, Yixin Xu, Aitor Pellicer Camardiel, Daniel Zhang, Allen Xue, Amol Aher, Ellie Walker, Florina Marxer, Tarun M Kapoor, Michal Wieczorek","doi":"10.1083/jcb.202410206","DOIUrl":"10.1083/jcb.202410206","url":null,"abstract":"The γ-tubulin ring complex (γ-TuRC) is an essential multiprotein assembly that provides a template for microtubule nucleation. The γ-TuRC is recruited to microtubule-organizing centers (MTOCs) by the evolutionarily conserved attachment factor NEDD1. However, the structural basis of the NEDD1-γ-TuRC interaction is not known. Here, we report cryo-EM structures of NEDD1 bound to the human γ-TuRC in the absence or presence of the activating factor CDK5RAP2. We found that the C-terminus of NEDD1 forms a tetrameric α-helical assembly that contacts the lumen of the γ-TuRC cone and orients its microtubule-binding domain away from the complex. The structure of the γ-TuRC simultaneously bound to NEDD1 and CDK5RAP2 reveals that both factors can associate with the \"open\" conformation of the complex. Our results show that NEDD1 does not induce substantial conformational changes in the γ-TuRC but suggest that anchoring of γ-TuRC-capped microtubules by NEDD1 would be structurally compatible with the significant conformational changes experienced by the γ-TuRC during microtubule nucleation.","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/PMC12094035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110599","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

A coordinated kinase and phosphatase network regulates Stu2 recruitment to yeast kinetochores. 一个协调的激酶和磷酸酶网络调节着Stu2向酵母着丝点的募集。

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.202410196

Michael G Stewart, Joseph S Carrier, Jacob A Zahm, Stephen C Harrison, Matthew P Miller

{"title":"A coordinated kinase and phosphatase network regulates Stu2 recruitment to yeast kinetochores.","authors":"Michael G Stewart, Joseph S Carrier, Jacob A Zahm, Stephen C Harrison, Matthew P Miller","doi":"10.1083/jcb.202410196","DOIUrl":"10.1083/jcb.202410196","url":null,"abstract":"Cells coordinate diverse events at anaphase onset, including separase activation, cohesin cleavage, chromosome separation, and spindle reorganization. Regulation of the XMAP215 family member and microtubule polymerase, Stu2, at the metaphase-anaphase transition determines a redistribution from kinetochores to spindle microtubules. We show that cells modulate Stu2 kinetochore-microtubule localization by Polo-like kinase1/Cdc5-mediated phosphorylation of T866, near the Stu2 C-terminus, thereby promoting dissociation from the kinetochore Ndc80 complex. Cdk/Cdc28 likely primes Cdc5:Stu2 interaction. Cdc28 activity is also required for Stu2 nuclear import. PP2ACdc55 actively opposes Cdc5 activity on Stu2T866 during metaphase. This counter-regulation allows for switch-like redistribution of Stu2pT866 at anaphase onset when separase inhibits PP2ACdc55. Blocking Stu2T866 phosphorylation disrupts anaphase spindle progression, and we infer that PP2ACdc55 regulates the mitotic spindle by dephosphorylating multiple MAPs, including Stu2. These data support a model in which increased phosphorylation at anaphase onset results from phosphatase inhibition and point to a larger regulatory network that facilitates rapid cytoskeletal modulation required for anaphase spindle function.","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/PMC12203985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505822","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

Spindle morphology changes between meiosis and mitosis driven by CK2 regulation of the Ran pathway. CK2调控Ran通路驱动减数分裂和有丝分裂纺锤体形态的变化。

IF 7.4 1区生物学

Journal of Cell Biology Pub Date : 2025-08-04 Epub Date: 2025-07-01 DOI: 10.1083/jcb.202407154

Helena Cantwell, Hieu Nguyen, Arminja N Kettenbach, Rebecca Heald

{"title":"Spindle morphology changes between meiosis and mitosis driven by CK2 regulation of the Ran pathway.","authors":"Helena Cantwell, Hieu Nguyen, Arminja N Kettenbach, Rebecca Heald","doi":"10.1083/jcb.202407154","DOIUrl":"10.1083/jcb.202407154","url":null,"abstract":"The transition from meiotic divisions in the oocyte to embryonic mitoses is a critical step in animal development. Despite negligible changes to cell size and shape, following fertilization the small, barrel-shaped meiotic spindle is replaced by a large zygotic spindle that nucleates abundant astral microtubules at spindle poles. To probe underlying mechanisms, we applied a drug treatment approach using Ciona eggs and found that inhibition of casein kinase 2 (CK2) caused a shift from meiotic to mitotic-like spindle morphology with nucleation of robust astral microtubules, an effect reproduced in Xenopus egg cytoplasmic extracts. In both species, CK2 activity decreased at fertilization. Phosphoproteomic differences between Xenopus meiotic and mitotic extracts that also accompanied CK2 inhibition pointed to RanGTP-regulated factors as potential targets. Interfering with RanGTP-driven microtubule formation suppressed astral microtubule growth caused by CK2 inhibition. These data support a model in which CK2 activity attenuation at fertilization leads to activation of RanGTP-regulated microtubule effectors, inducing mitotic spindle morphology.","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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540342","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