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Molecular and Cellular Biology, January 2004, p. 719-729, Vol. 24, No. 2
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.2.719-729.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Immunological Function in Mice Lacking the Rac-Related GTPase RhoG

Elena Vigorito,1* Sarah Bell,1 Barbara J. Hebeis,1 Helen Reynolds,1 Simon McAdam,1 Piers C. Emson,2 Andrew McKenzie,3 and Martin Turner1

Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme,1 Laboratory of Molecular Neuroscience, The Babraham Institute, Babraham, Cambridge CB2 4AT,2 Laboratory for Molecular Biology, Hills Road, Cambridge CB2 2QM, United Kingdom3

Received 25 March 2003/ Returned for modification 22 April 2003/ Accepted 20 October 2003

RhoG is a low-molecular-weight GTPase highly expressed in lymphocytes that activates gene transcription and promotes cytoskeletal reorganization in vitro. To study the in vivo function of RhoG, we generated mice homozygous for a targeted disruption of the RhoG gene. Despite the absence of RhoG, the development of B and T lymphocytes was unaffected. However, there was an increase in the level of serum immunoglobulin G1 (IgG1) and IgG2b as well as a mild increase of the humoral immune response to thymus-dependent antigens. In addition, B- and T-cell proliferation in response to antigen receptor cross-linking was slightly increased. Although RhoG deficiency produces a mild phenotype, our experiments suggest that RhoG may contribute to the negative regulation of immune responses. The lack of a strong phenotype could indicate a functional redundancy of RhoG with other Rac proteins in lymphocytes.

* Corresponding author. Mailing address: Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, United Kingdom. Phone: 44 1223 496 545. Fax: 44 1223 496 023. E-mail: elena.vigorito{at}bbsrc.ac.uk.

Molecular and Cellular Biology, January 2004, p. 719-729, Vol. 24, No. 2
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.2.719-729.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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