C. elegans G Protein Regulator RGS-3 Controls Sensitivity to Sensory Stimuli

Denise M. Ferkey, Rhonda Hyde, Gal Haspel, Heather M. Dionne, Heather A. Hess, Hiroshi Suzuki, William R. Schafer, Michael R. Koelle, Anne C. Hart

Research output: Contribution to journalArticlepeer-review

50 Scopus citations


Signal transduction through heterotrimeric G proteins is critical for sensory response across species. Regulator of G protein signaling (RGS) proteins are negative regulators of signal transduction. Herein we describe a role for C. elegans RGS-3 in the regulation of sensory behaviors. rgs-3 mutant animals fail to respond to intense sensory stimuli but respond normally to low concentrations of specific odorants. We find that loss of RGS-3 leads to aberrantly increased G protein-coupled calcium signaling but decreased synaptic output, ultimately leading to behavioral defects. Thus, rgs-3 responses are restored by decreasing G protein-coupled signal transduction, either genetically or by exogenous dopamine, by expressing a calcium-binding protein to buffer calcium levels in sensory neurons or by enhancing glutamatergic synaptic transmission from sensory neurons. Therefore, while RGS proteins generally act to downregulate signaling, loss of a specific RGS protein in sensory neurons can lead to defective responses to external stimuli.

Original languageEnglish (US)
Pages (from-to)39-52
Number of pages14
Issue number1
StatePublished - Jan 4 2007
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • General Neuroscience




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