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MBC in Press, published online ahead of print July 18, 2007
Mol. Biol. Cell 10.1091/mbc.E07-03-0281

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Submitted on March 27, 2007
Revised on June 29, 2007
Accepted on July 6, 2007

Inactivation of Rho GTPases with Clostridium difficile Toxin B Impairs Centrosomal Activation of Aurora-A in G2/M Transition of HeLa Cells

Yoshikazu Ando,* Shingo Yasuda,*{dagger} Fabian Oceguera-Yanez,* and Shuh Narumiya*

*Department of Pharmacology and {dagger}Horizontal Medical Research Organization, Kyoto University Faculty of Medicine, Kyoto 606-8501, Japan

Monitoring Editor: Yixian Zheng

During G2 phase of cell cycle, centrosomes function as a scaffold for activation of mitotic kinases. Aurora-A is first activated at late G2 phase at the centrosome, facilitates centrosome maturation, and induces activation of cyclin B-Cdk1 at the centrosome for mitotic entry. While several molecules including HEF1 and PAK are implicated in centrosomal activation of Aurora-A, signaling pathways leading to Aurora-A activation at the centrosome and hence mitotic commitment in vertebrate cells remain largely unknown. Here, we have used Clostridium difficile toxin B, and examined the role of Rho GTPases in G2/M transition of HeLa cells. Inactivation of Rho GTPases by the toxin B treatment delayed by two hours histone H3 phosphorylation, Cdk1/cyclin B activation and Aurora-A activation. Furthermore, PAK activation at the centrosome that was already present before the toxin addition was significantly attenuated for two hours by the addition of toxin B, and HEF1 accumulation at the centrosome that occurred in late G2 phase was also delayed. These results suggest that Rho GTPases function in G2/M transition of mammalian cells by mediating multiple signaling pathways converging to centrosomal activation of Aurora-A.

Address correspondence to: Shuh Narumiya (snaru{at}mfour.med.kyoto-u.ac.jp)




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[Abstract] [Full Text] [PDF]


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