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Gene Review

goa-1  -  Protein GOA-1

Caenorhabditis elegans

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Psychiatry related information on goa-1

  • Mutations in goa-1, dgk-1, eat-16, or eat-11 strongly or completely suppressed unc-43(gf) lethargy, but affected other mutants with reduced locomotion only weakly [1].

High impact information on goa-1

  • 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 [2].
  • Mutations in the goa-1 gene, which encodes an alpha subunit of Go (G alpha o), cause behavioral defects similar to those observed in mutants that lack the neurotransmitter serotonin (5-HT), and goa-1 mutants are partially resistant to exogenous 5-HT [3].
  • Animals defective in either gene display a hyperactive phenotype similar to that of goa-1 loss-of-function mutants [4].
  • Mutants lacking goa-1 G(alpha)0 accumulated abnormally high levels of the DAG-binding protein UNC-13 at motor neuron nerve terminals, suggesting that serotonin inhibits synaptic transmission by decreasing the abundance of UNC-13 at release sites [5].
  • RIC-8 was genetically shown to act in concert with goa-1 to regulate centrosome movements in C. elegans . Interestingly, mammalian RIC-8 was recently found to behave as a GEF for Galpha subunits in vitro . We show that reduction of function of ric-8 results in a 1 cell embryo phenotype very similar to the phenotype of embryos depleted of Galpha [6].

Biological context of goa-1

  • In ric-8 reduction of function backgrounds, the embryonic lethality, spindle misalignments and delayed nuclear migration are strongly enhanced by a 50% reduction in maternal goa-1 gene dosage [7].
  • The system allows comparison of distinct genotypes that affect movement similarly (activation of Gq-alpha versus loss of Go-alpha function), as well as of different mutant alleles at a single locus (null and dominant negative alleles of the goa-1 gene, which encodes Go-alpha) [8].

Anatomical context of goa-1

  • Through Nomarski analysis we show that goa-1 and ric-8 mutant embryos exhibit defects in multiple events that involve centrosomes, including one-cell posterior centrosome rocking, P(1) centrosome flattening, mitotic spindle alignment, and nuclear migration [7].

Associations of goa-1 with chemical compounds

  • Loss-of-function mutants of the gene goa-1, which codes for the alpha-subunit of Go, have EC(50)s for the VA isoflurane of 1.7- to 2.4-fold that of wild type [9].
  • The RGS overexpressing strains, a goa-1 missense mutant found to carry a novel mutation near the GTP-binding domain, and eat-16(rf) mutants, which suppress goa-1(gf) mutations, are all halothane resistant; goa-1(null) mutants have wild-type sensitivities [9].

Other interactions of goa-1

  • Interestingly, these characteristic defects resembled phenotypes observed in gain-of-function mutants of unc-43/Ca(2+)-calmodulin-dependent protein kinase II (CaMKII) and goa-1/G(o)-protein alpha-subunit [10].
  • Strains overexpressing egl-10, which codes for an RGS protein negatively regulating goa-1, are also isoflurane resistant [9].


  1. Calcium/calmodulin-dependent protein kinase II regulates Caenorhabditis elegans locomotion in concert with a G(o)/G(q) signaling network. Robatzek, M., Thomas, J.H. Genetics (2000) [Pubmed]
  2. Participation of the protein Go in multiple aspects of behavior in C. elegans. Mendel, J.E., Korswagen, H.C., Liu, K.S., Hajdu-Cronin, Y.M., Simon, M.I., Plasterk, R.H., Sternberg, P.W. Science (1995) [Pubmed]
  3. Modulation of serotonin-controlled behaviors by Go in Caenorhabditis elegans. Ségalat, L., Elkes, D.A., Kaplan, J.M. Science (1995) [Pubmed]
  4. Antagonism between G(o)alpha and G(q)alpha in Caenorhabditis elegans: the RGS protein EAT-16 is necessary for G(o)alpha signaling and regulates G(q)alpha activity. Hajdu-Cronin, Y.M., Chen, W.J., Patikoglou, G., Koelle, M.R., Sternberg, P.W. Genes Dev. (1999) [Pubmed]
  5. Serotonin inhibition of synaptic transmission: Galpha(0) decreases the abundance of UNC-13 at release sites. Nurrish, S., Ségalat, L., Kaplan, J.M. Neuron (1999) [Pubmed]
  6. Control of embryonic spindle positioning and Galpha activity by C. elegans RIC-8. Couwenbergs, C., Spilker, A.C., Gotta, M. Curr. Biol. (2004) [Pubmed]
  7. A role for RIC-8 (Synembryn) and GOA-1 (G(o)alpha) in regulating a subset of centrosome movements during early embryogenesis in Caenorhabditis elegans. Miller, K.G., Rand, J.B. Genetics (2000) [Pubmed]
  8. An automated system for measuring parameters of nematode sinusoidal movement. Cronin, C.J., Mendel, J.E., Mukhtar, S., Kim, Y.M., Stirbl, R.C., Bruck, J., Sternberg, P.W. BMC Genet. (2005) [Pubmed]
  9. Goalpha regulates volatile anesthetic action in Caenorhabditis elegans. van Swinderen, B., Metz, L.B., Shebester, L.D., Mendel, J.E., Sternberg, P.W., Crowder, C.M. Genetics (2001) [Pubmed]
  10. Calcineurin, a calcium/calmodulin-dependent protein phosphatase, is involved in movement, fertility, egg laying, and growth in Caenorhabditis elegans. Bandyopadhyay, J., Lee, J., Lee, J., Lee, J.I., Yu, J.R., Jee, C., Cho, J.H., Jung, S., Lee, M.H., Zannoni, S., Singson, A., Kim, d.o. .H., Koo, H.S., Ahnn, J. Mol. Biol. Cell (2002) [Pubmed]
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