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Published online 10 January 2005. doi:10.1083/jcb.200408085
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 168, Number 2, 221-232
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Article

Ect2 and MgcRacGAP regulate the activation and function of Cdc42 in mitosis



Fabian Oceguera-Yanez1,2, Kazuhiro Kimura1, Shingo Yasuda1,2, Chiharu Higashida1, Toshio Kitamura3, Yasushi Hiraoka4,5, Tokuko Haraguchi4,5, and Shuh Narumiya1

1 Department of Pharmacology, Kyoto University Faculty of Medicine, Kyoto 606-8501, Japan
2 Horizontal Medical Research Organization, Kyoto University Faculty of Medicine, Kyoto 606-8501, Japan
3 Division of Cellular Therapy, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan
4 Core Research for Evolutionary Science and Technology Research Project, Kansai Advanced Research Center, Kobe 651-2492, Japan
5 Department of Biology, Graduate School of Science, Osaka University, Osaka 560-0043, Japan

Correspondence to Shuh Narumiya: snaru{at}mfour.med.kyoto-u.ac.jp

Although Rho regulates cytokinesis, little was known about the functions in mitosis of Cdc42 and Rac. We recently suggested that Cdc42 works in metaphase by regulating bi-orient attachment of spindle microtubules to kinetochores. We now confirm the role of Cdc42 by RNA interference and identify the mechanisms for activation and down-regulation of Cdc42. Using a pull-down assay, we found that the level of GTP-Cdc42 elevates in metaphase, whereas the level of GTP-Rac does not change significantly in mitosis. Overexpression of dominant-negative mutants of Ect2 and MgcRacGAP, a Rho GTPase guanine nucleotide exchange factor and GTPase activating protein, respectively, or depletion of Ect2 by RNA interference suppresses this change of GTP-Cdc42 in mitosis. Depletion of Ect2 also impairs microtubule attachment to kinetochores and causes prometaphase delay and abnormal chromosomal segregation, as does depletion of Cdc42 or expression of the Ect2 and MgcRacGAP mutants. These results suggest that Ect2 and MgcRacGAP regulate the activation and function of Cdc42 in mitosis.

K. Kimura's present address is Dept. of Ophthalmology, Yamaguchi University School of Medicine, Yamaguchi 755-8505, Japan.

Abbreviations used in this paper: CRIB, Cdc42-Rac–interacting binding domain; DH, Dbl homology; GAP, GTPase activating protein; GEF, guanine nucleotide exchange factor; MT, microtubule; PH, pleckstrin homology; RNAi, RNA interference.


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