Polo-like kinase 1 promotes Cdc42-induced actin polymerization for asymmetric division in oocytes
Wai Shan Yuen,
Qing Hua Zhang,
Anne Bourdais,
Deepak Adhikari,
Guillaume Halet,
John Carroll
Affiliations
Wai Shan Yuen
Department of Anatomy and Developmental Biology and Development and Stem Cells Program, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia
Qing Hua Zhang
Department of Anatomy and Developmental Biology and Development and Stem Cells Program, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia
Anne Bourdais
University of Rennes, CNRS, IGDR - UMR 6290, F-35000 Rennes, France
Deepak Adhikari
Department of Anatomy and Developmental Biology and Development and Stem Cells Program, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia
Guillaume Halet
University of Rennes, CNRS, IGDR - UMR 6290, F-35000 Rennes, France
John Carroll
Department of Anatomy and Developmental Biology and Development and Stem Cells Program, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia
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.
