Polo-like kinase 1 promotes Cdc42-induced actin polymerization for asymmetric division in oocytes

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.

KIF2A Upregulates PI3K/AKT Signaling through Polo-like Kinase 1 (PLK1) to Affect the Proliferation and Apoptosis Levels of Eriocheir sinensis Spermatogenic Cells

“…For example, PLK1 mediates the phosphorylation of specific substrates and participates in a series of important cellular activities, such as nuclear membrane breakdown (NEBD), centrosome maturation, spindle assembly, chromosome segregation, and cytokinesis [ 25 , 26 , 27 ]. In oocytes, PLK1 promotes actin polymerization induced by polarity protein Cdc42 and promotes asymmetric oocyte division [ 28 ]. In addition, PLK1 knockdown ameliorates testicular epithelial cell apoptosis and the intestinal barrier during sepsis.…”