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Fitzgerald, K. et al.

Chemical genetics reveals an RGS/ G-protein role in the action of a compound.

We report here on a chemical genetic screen designed to address the mechanism of action of a small molecule. Small molecules that were active in models of urinary incontinence were tested on the nematode Caenorhabditis elegans, and the resulting phenotypes were used as readouts in a genetic screen to identify possible molecular targets. The mutations giving resistance to compound were found to affect members of the RGS protein/ G-protein complex. Studies in mammalian systems confirmed that the small molecules inhibit muscarinic G-protein coupled receptor (GPCR) signaling involving G-alphaq (G-protein alpha subunit). Our studies suggest that the small molecules act at the level of the RGS/G-alphaq signaling complex, and define new mutations in both RGS and G-alphaq, including a unique hypo-adapation allele of G-alphaq. These findings suggest that therapeutics targeted to downstream components of GPCR signaling may be effective for treatment of diseases involving inappropriate receptor activation.[1]

References

Chemical genetics reveals an RGS/G-protein role in the action of a compound. Fitzgerald, K., Tertyshnikova, S., Moore, L., Bjerke, L., Burley, B., Cao, J., Carroll, P., Choy, R., Doberstein, S., Dubaquie, Y., Franke, Y., Kopczynski, J., Korswagen, H., Krystek, S.R., Lodge, N.J., Plasterk, R., Starrett, J., Stouch, T., Thalody, G., Wayne, H., van der Linden, A., Zhang, Y., Walker, S.G., Cockett, M., Wardwell-Swanson, J., Ross-Macdonald, P., Kindt, R.M. PLoS Genet. (2006) [Pubmed]

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