Inhibition of Cdc42 during mitotic exit is required for cytokinesis |
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| Authors: | Benjamin D Atkins Satoshi Yoshida Koji Saito Chi-Fang Wu Daniel J Lew David Pellman |
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| Institution: | 1.Department of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115;2.Department of Biology, and 3.Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, MA 02454;4.Howard Hughes Medical Institute, Chevy Chase, MD 20815;5.Department of Pharmacology and Cancer Biology, Duke University, Durham, NC 27710 |
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| Abstract: | The role of Cdc42 and its regulation during cytokinesis is not well understood. Using biochemical and imaging approaches in budding yeast, we demonstrate that Cdc42 activation peaks during the G1/S transition and during anaphase but drops during mitotic exit and cytokinesis. Cdc5/Polo kinase is an important upstream cell cycle regulator that suppresses Cdc42 activity. Failure to down-regulate Cdc42 during mitotic exit impairs the normal localization of key cytokinesis regulators—Iqg1 and Inn1—at the division site, and results in an abnormal septum. The effects of Cdc42 hyperactivation are largely mediated by the Cdc42 effector p21-activated kinase Ste20. Inhibition of Cdc42 and related Rho guanosine triphosphatases may be a general feature of cytokinesis in eukaryotes. |
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