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Infection and Immunity, October 2001, p. 6271-6275, Vol. 69, No. 10
Department of Microbiology and Immunology,
Stanford University School of Medicine, Stanford, California
Received 7 May 2001/Accepted 7 July 2001
Pathogens produce virulence factors that interact
directly with host molecules, but in many cases the host
targets are unknown. The genetic and molecular identification of these
orphan targets is often not feasible with mammalian experimental
models. However, a substantial number of known targets are molecules
and pathways that are conserved among eukaryotes, and therefore the use
of nonmammalian model hosts to identify orphan targets may prove useful. To demonstrate the feasibility of this approach, we transformed the nematode Caenorhabditis elegans with a gene
encoding the catalytic subunit of pertussis toxin (PTX), which in
mammals inactivates Go/i
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.10.6271-6275.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Mimicry of a G Protein Mutation by Pertussis Toxin
Expression in Transgenic Caenorhabditis elegans
proteins. Expression of PTX in
C. elegans produced phenotypes almost identical to
those of a null mutation in the nematode gene encoding
Go/i
. Furthermore, PTX suppressed the phenotype of a constitutively active form of nematode Go/i
protein.
These results indicate that PTX is functional in nematodes and acts
specifically on the C. elegans homologue of the
mammalian target.
*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, Stanford University School of Medicine, 299 Campus Dr., Stanford, CA 94305-5124. Phone: (650) 723-2671. Fax:
(650) 723-1837. E-mail: cdarby{at}stanford.edu.
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