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Gene Review: 

eat-16  -  Protein EAT-16

Caenorhabditis elegans

 
 
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High impact information on eat-16

  • Animals defective in both sag-1 and eat-16 are inviable, but reducing function in egl-30 restores viability, indicating that the lethality of the eat-16; sag-1 double mutant is due to excessive G(q)alpha activity [1].
  • Double-mutant analysis indicates that both sag-1 and eat-16 act downstream of, or parallel to, G(o)alpha and negatively regulate EGL-30 (G(q)alpha) signaling. eat-16 encodes a regulator of G protein signaling (RGS) most similar to the mammalian RGS7 and RGS9 proteins and can inhibit endogenous mammalian G(q)/G(11) in COS-7 cells [1].
  • Either overexpression of the C. elegans Galpha subunit odr-3 or loss of eat-16, which encodes a regulator of G protein signaling (RGS) protein, restores chemosensation in Ce-grk-2 mutants [2].
  • GPB-2 protein is nearly absent in eat-16; egl-10 double mutants, and EGL-10 protein is severely diminished in gpb-2 mutants [3].

References

  1. 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]
  2. G protein-coupled receptor kinase function is essential for chemosensation in C. elegans. Fukuto, H.S., Ferkey, D.M., Apicella, A.J., Lans, H., Sharmeen, T., Chen, W., Lefkowitz, R.J., Jansen, G., Schafer, W.R., Hart, A.C. Neuron (2004) [Pubmed]
  3. Two RGS proteins that inhibit Galpha(o) and Galpha(q) signaling in C. elegans neurons require a Gbeta(5)-like subunit for function. Chase, D.L., Patikoglou, G.A., Koelle, M.R. Curr. Biol. (2001) [Pubmed]
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