This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Masuda, M. Articles by Horiguchi, Y. Search for Related Content PubMed PubMed Citation Articles by Masuda, M. Articles by Horiguchi, Y.

 Previous Article  |  Next Article 

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.

---

* Corresponding author. Mailing address: Department of Bacterial Toxinology, Research Institute for Microbial Diseases, Osaka University, Yamada-oka 3-1, Suita, Osaka 565-0871, Japan. Phone: 81-6-6879-8284. Fax: 81-6-6879-8283. E-mail: horiguti{at}0040biken.osaka-u.ac.jp.

Editor: J. T. Barbieri

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

---

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.

This article has been cited by other articles:

• Harriff, M. J., Danelishvili, L., Wu, M., Wilder, C., McNamara, M., Kent, M. L., Bermudez, L. E. (2009). Mycobacterium avium Genes MAV_5138 and MAV_3679 Are Transcriptional Regulators That Play a Role in Invasion of Epithelial Cells, in Part by Their Regulation of CipA, a Putative Surface Protein Interacting with Host Cell Signaling Pathways. J. Bacteriol. 191: 1132-1142 [Abstract] [Full Text]  
• Fukui, A., Horiguchi, Y. (2004). Bordetella Dermonecrotic Toxin Exerting Toxicity through Activation of the Small GTPase Rho. J Biochem 136: 415-419 [Abstract] [Full Text]  
• Matsuzawa, T., Fukui, A., Kashimoto, T., Nagao, K., Oka, K., Miyake, M., Horiguchi, Y. (2004). Bordetella Dermonecrotic Toxin Undergoes Proteolytic Processing to Be Translocated from a Dynamin-related Endosome into the Cytoplasm in an Acidification-independent Manner. J. Biol. Chem. 279: 2866-2872 [Abstract] [Full Text]  
• Matsuzawa, T., Kashimoto, T., Katahira, J., Horiguchi, Y. (2002). Identification of a Receptor-Binding Domain of Bordetella Dermonecrotic Toxin. Infect. Immun. 70: 3427-3432 [Abstract] [Full Text]