ArticleNature communications2019
Cdk1-mediated DIAPH1 phosphorylation maintains metaphase cortical tension and inactivates the spindle assembly checkpoint at anaphase.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 26 citations in OpenAlex.
- Glycation and receptors: coming of AGE in the midst of danger.Nature reviews. Endocrinology · 2026Review
- CDK1-mediated phosphorylation of EPLIN is crucial for mitotic spindle positioning.Communications biology · 2026Article
- ARHGEF17/TEM4 regulates the cell cycle through control of G1 progression.The Journal of cell biology · 2025Article
- Diaph1 knockout inhibits mouse primordial germ cell proliferation and affects gonadal development.Reproductive biology and endocrinology : RB&E · 2024Article
- Exosomal MicroRNAs: Biomarkers of moyamoya disease and involvement in vascular cytoskeleton reconstruction.Heliyon · 2024Article
- Mechanosensitive accumulation of non-muscle myosin IIB during mitosis requires its translocation activity.iScience · 2023Article
- Targeting CDK1 in cancer: mechanisms and implications.NPJ precision oncology · 2023Review
- Identification and characterization of the CDK1-BMAL1-UHRF1 pathway driving tumor progression.iScience · 2023Article
- Late-onset hearing loss case associated with a heterozygous truncating variant of DIAPH1.Clinical genetics · 2022Article
- LY6K-AS lncRNA is a lung adenocarcinoma prognostic biomarker and regulator of mitotic progression.Oncogene · 2021Article
- Host CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli.Nature communications · 2021Article
- Artificially decreasing cortical tension generates aneuploidy in mouse oocytes.Nature communications · 2020Article
- Review
- Remodeling of ER Membrane Contact Sites During Cell Division.Contact (Thousand Oaks (Ventura County, Calif.))Review
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Animal cells undergo rapid rounding during mitosis, ensuring proper chromosome segregation, during which an outward rounding force abruptly increases upon prometaphase entry and is maintained at a constant level during metaphase. Initial cortical tension is generated by the actomyosin system to which both myosin motors and actin network architecture contribute. However, how cortical tension is maintained and its physiological significance remain unknown. We demonstrate here that Cdk1-mediated phosphorylation of DIAPH1 stably maintains cortical tension after rounding and inactivates the spindle assembly checkpoint (SAC). Cdk1 phosphorylates DIAPH1, preventing profilin1 binding to maintain cortical tension. Mutation of DIAPH1 phosphorylation sites promotes cortical F-actin accumulation, increases cortical tension, and delays anaphase onset due to SAC activation. Measurement of the intra-kinetochore length suggests that Cdk1-mediated cortex relaxation is indispensable for kinetochore stretching. We thus uncovered a previously unknown mechanism by which Cdk1 coordinates cortical tension maintenance and SAC inactivation at anaphase onset.
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