egl-30 encodes a G protein a subunit which is more than 80% identical to two members of the mammalian Gqa family[1]. We are interested in genes which act in the
egl-30 pathway, as they may encode new regulators of G protein signalling.
eat-11 is one such gene.
eat-11 animals arrest at hatching in the presence of low levels of the cholinergic agonist arecoline[2] and mutations in
egl-30 strongly suppress this arecoline effect[1]. We have found that
eat-11 animals exhibit behaviors which are opposite to
egl-30(r.f). animals in several respects.
egl-30(r.f.) animals move slowly and with reduced flexations, and lay few eggs in the presence of serotonin. By contrast,
eat-11 animals move more quickly than wild type animals and with exaggerated flexations. In addition,
eat-11 animals respond dramatically more strongly than N2 to serotonin in an egg laying assay. We hope to clarify the relationship between
egl-30 and
eat-11 by determining the molecular identity of the EAT-11 protein. [1] Brundage, L. ,Avery, L., Katz, A., Kim, U-J., Mendel, J.E., Sternberg, P. W., and Simon, M.I. (1996) Mutations in a C. elegans Gqa gene disrupt movement, egg laying, and viability. Neuron 16: 999-1009. [2] Avery, L. (1993) The genetics of feeding in Caenorhabditis elegans. Genetics 133: 897-917.