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

Neuron. 1996 May;16(5):999-1009. doi: 10.1016/s0896-6273(00)80123-3.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Arecoline / pharmacology
  • Base Sequence
  • Caenorhabditis elegans / physiology*
  • DNA Primers / chemistry
  • Female
  • GTP-Binding Proteins / genetics*
  • Molecular Sequence Data
  • Movement
  • Muscle Contraction
  • Mutation
  • Oviposition*
  • Sequence Alignment
  • Sequence Homology, Amino Acid

Substances

  • DNA Primers
  • Arecoline
  • GTP-Binding Proteins

Associated data

  • GENBANK/U56864