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Infection and Immunity, February 2002, p. 998-1001, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.998-1001.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

In Vivo Modifications of Small GTPase Rac and Cdc42 by Bordetella Dermonecrotic Toxin

Minako Masuda,^, Masayoshi Minami, Hiroaki Shime, Takeshi Matsuzawa, and Yasuhiko Horiguchi^*

Department of Bacterial Toxinology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan

Received 10 September 2001/ Returned for modification 10 October 2001/ Accepted 7 November 2001

Bordetella dermonecrotic toxin (DNT) is known to activate the small GTPase Rho through deamidation or polyamination. In this study, we examined whether Rac and Cdc42, the two other members of the Rho family, serve as intracellular targets for the toxin. Immunoprecipitation and immunoblot assays revealed that DNT deamidated or polyaminated intracellular Rac and Cdc42. After the modifications, both Rac and Cdc42 lost their GTP-hydrolyzing, but not GTP-binding, activities. The interactions of the modified Rac and Cdc42 with their respective effectors were strictly dependent on GTP. MC3T3-E1 cells treated with DNT at high concentrations demonstrated extensive formations of lamellipodia and filopodia, which indicate the intracellular activation of Rac and Cdc42, respectively.

Editor: J. T. Barbieri

Present address: Department of Molecular Cell Biology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan

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