Open AccessIn Vivo Modifications of Small GTPase Rac and Cdc42 by Bordetella Dermonecrotic Toxin
Author(s) -
Minako Masuda,
M. Minami,
Hiroaki Shime,
Takeshi Matsuzawa,
Yasuhiko Horiguchi
Publication year - 2002
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.70.2.998-1001.2002
Subject(s) - cdc42 , gtpase , biology , intracellular , filopodia , microbiology and biotechnology , gtp' , toxin , bordetella , clostridium difficile toxin b , small gtpase , rac1 , biochemistry , clostridium difficile toxin a , bordetella pertussis , actin , signal transduction , bacteria , genetics , clostridium difficile , enzyme , antibiotics
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.