High impact information on G-protein

• Two previously known and 13 newly identified mammalian genes have similarity to egl-10 and SST2, and we propose that members of this family regulate many G protein signaling pathways [1].
• Different G-protein signaling pathways have characteristic effects on behavior, neuronal degeneration, and embryonic development [2].
• The goa-1 gene encoding the alpha subunit of the heterotrimeric guanosine triphosphate-binding protein (G protein) Go from Caenorhabditis elegans is expressed in most neurons, and in the muscles involved in egg laying and male mating [3].
• To elucidate the cellular role of the heterotrimeric G protein G(o), we have taken a molecular genetic approach in Caenorhabditis elegans [4].
• 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 [5].

Biological context of G-protein

• G-protein signaling plays important roles in asymmetric cell division [6].
• Chemical genetics reveals an RGS/G-protein role in the action of a compound [7].
• 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 [5].
• Our results indicate that, along with CaMKII, calcineurin regulates G-protein-coupled phosphorylation signaling pathways in C.elegans [8].
• Noncell- and cell-autonomous G-protein-signaling converges with Ca2+/mitogen-activated protein kinase signaling to regulate str-2 receptor gene expression in Caenorhabditis elegans [9].

Anatomical context of G-protein

• These channels, as well as the G-protein Galpha(o), function in neuroendocrine cells to promote release of neurotransmitters that block egg laying until eggs filling the uterus deform the neuroendocrine cells [10].
• AF2 interaction with Ascaris suum body wall muscle membranes involves G-protein activation [11].
• CONCLUSIONS: Our findings show that oocyte Eph receptor and somatic cell G protein signaling pathways control meiotic diapause in C. elegans, highlighting contrasts and parallels between MSP signaling in C. elegans and luteinizing hormone signaling in mammals [12].

Associations of G-protein with chemical compounds

• Among the three G-protein-linked acetylcholine receptors (GARs) in Caenorhabditis elegans (C. elegans), GAR-3 is structurally and pharmacologically most similar to mammalian muscarinic acetylcholine receptors (mAChRs) [13].
• mGluRs (metabotropic glutamate receptors) are G-protein-coupled receptors that play an important neuromodulatory role in the brain [14].
• This paper is the first comprehensive study of G protein-coupled serotonin receptors of C. elegans [15].

Other interactions of G-protein

• The signaling cascade is only partially dependent on the phospholipase C beta (EGL-8) and is negatively regulated by G alpha(o) [GOA-1 (G-protein, O, alpha subunit family member 1)] and calcium/calmodulin-dependent kinase [UNC-43 (uncoordinated family member 43)] [16].
• RNAi depletion of gpr-1 and gpr-2, homologs of mammalian AGS3 and Drosophila PINS (receptor-independent G protein regulators), results in a phenotype identical to that of embryos depleted of both GPA-16 and GOA-1; the first cleavage is symmetric, but polarity is not affected [17].
• To further analyze Galpha(o) signaling, we cloned the egl-47 gene, which was identified by two dominant mutations that severely inhibit egg laying. egl-47 encodes two orphan G-protein-coupled receptor isoforms, which share all seven transmembrane domains but have different extracellular N termini [18].
• Here we show that the same Ca2+/MAPK pathway promotes str-2 expression in the AWC and ASI neurons together with multiple cell-autonomous and noncell-autonomous G-protein-signaling pathways [9].
• MAU-8 is a Phosducin-like Protein required for G protein signaling in C. elegans [19].

References