Two RGS proteins that inhibit Gαo and Gαq signaling in C. elegans neurons require a Gβ5-like subunit for function

Abstract

Gbeta(5) functions in vivo complexed with GGL-containing RGS proteins. In the absence of Gbeta(5), these RGS proteins have little or no function. The formation of RGS-Gbeta(5) complexes is required for the expression or stability of both the RGS and Gbeta(5) proteins. Appropriate RGS-Gbeta(5) complexes regulate both Galpha(o) and Galpha(q) proteins in vivo.

Identification and molecular characterization of the Gα12–Rho guanine nucleotide exchange factor pathway in Caenorhabditis elegans

“…Because TPA-1 can be activated by the G␣q-PLC pathway, the data also suggest a possible connection between the G␣12 and G␣q pathways in vivo. The network formation between different G protein-mediated pathways in vivo, such as the Gq and Go pathways, has previously been reported in C. elegans (35,36).…”

The Expanding Roles of GβγSubunits in G Protein–Coupled Receptor Signaling and Drug Action

“…Regarding GPB-2, this vertebrate Gb 5 homolog has been shown to bind Gg2like (GGL) domains containing regulator of G protein signaling (RGS) proteins, much like its vertebrate counterparts, suggesting it may also regulate the GTPase activity of Ga subunits (Chase et al, 2001;Robatzek et al, 2001;van der Linden et al, 2001). GPC-2 shows ubiquitous expression in C. elegans, and is most related to the vertebrate Gg 13 , which is least similar to all of the other Gg subunits in humans (see Table 2).…”

Resistance to Volatile Anesthetics by Mutations Enhancing Excitatory Neurotransmitter Release in Caenorhabditis elegans

“…Therefore, the isolated suppressor mutants are unlikely to belong to this second class of suptent with goa-1 acting antagonistically to EGL-30 to regulate cholinergic neurotransmitter release and VA sensipressors. The third class of suppressors could act by enhancing tivity (Hajdu-Cronin et al 1999;Lackner et al 1999;Miller et al 1999;Chase et al 2001; cholinergic neurotransmission regardless of the nature of the syntaxin allele. On the basis of the aldicarb-hyper-2001; van der Linden et al 2001;van Swinderen et al 2001).…”