ArticleOpen biology2023
Polo-like kinase 1 promotes Cdc42-induced actin polymerization for asymmetric division in oocytes.
Article in Open biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- From Cytoskeletal Remodeling to Oocyte Quality: The Emerging Role of Mechanics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Oocyte Kinetochores at the Nexus of Meiotic Drive and Segregation Fidelity.Advances in experimental medicine and biology · 2026Review
- Sirtuin 5-driven meiotic spindle assembly and actin-based migration in mouse oocyte meiosis.Heliyon · 2024Article
- KIF2A Upregulates PI3K/AKT Signaling through Polo-like Kinase 1 (PLK1) to Affect the Proliferation and Apoptosis Levels ofBiology · 2024Article
- Polo-like kinase 1 promotes Cdc42-induced actin polymerization for asymmetric division in oocytes.Open biology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polo-like kinase I (Plk1) is a highly conserved seronine/threonine kinase essential in meiosis and mitosis for spindle formation and cytokinesis. Here, through temporal application of Plk1 inhibitors, we identify a new role for Plk1 in the establishment of cortical polarity essential for highly asymmetric cell divisions of oocyte meiosis. Application of Plk1 inhibitors in late metaphase I abolishes pPlk1 from spindle poles and prevents the induction of actin polymerization at the cortex through inhibition of local recruitment of Cdc42 and Neuronal Wiskott-Aldrich Syndrome protein (N-WASP). By contrast, an already established polar actin cortex is insensitive to Plk1 inhibitors, but if the polar cortex is first depolymerized, Plk1 inhibitors completely prevent its restoration. Thus, Plk1 is essential for establishment but not maintenance of cortical actin polarity. These findings indicate that Plk1 regulates recruitment of Cdc42 and N-Wasp to coordinate cortical polarity and asymmetric cell division.
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Registered trials
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