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Neuron. 1996 May;16(5):999-1009.

Mutations in a C. elegans Gqalpha gene disrupt movement, egg laying, and viability.

Author information

1
Division of Biology and Howard Hughes Medical Institute of Technology, Pasadena, California 91125, USA.

Abstract

We find that C. elegans egl-30 encodes a heterotrimeric G protein a subunit more than 80% identical to mammalian Gqalpha family proteins, and which can function as a Gqalpha subunit in COS-7 cells. We have identified new egl-30 alleles in a selection for genes involved in the C. elegans acetylcholine response. Two egl-30 alleles specify premature termination of Gqalpha and are essentially lethal in homozygotes. Animals homozygous for six other egl-30 alleles are viable and fertile, but exhibit delayed egg laying and leave flattened tracks. Overexpression of the wild-type egl-30 gene produces the opposite behavior. Analysis of these mutants suggest that their phenotypes reflect defects in the muscle or neuromuscular junction.

PMID:
8630258
PMCID:
PMC4444781
DOI:
10.1016/s0896-6273(00)80123-3
[Indexed for MEDLINE]
Free PMC Article

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