Mutations in a C. elegans Gqalpha gene disrupt movement, egg laying, and viability.
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.
Brundage
L
L
Division of Biology and Howard Hughes Medical Institute of Technology, Pasadena, California 91125, USA.
Avery
L
L
Katz
A
A
Kim
U J
UJ
Mendel
J E
JE
Sternberg
P W
PW
Simon
M I
MI
D000595:Amino Acid Sequence; D000818:Animals; D001115:Arecoline / Q000494:pharmacology; D001483:Base Sequence; D017173:Caenorhabditis elegans / Q000502:physiology*; D017931:DNA Primers / Q000737:chemistry; D005260:Female; D019204:GTP-Binding Proteins / Q000235:genetics*; D008969:Molecular Sequence Data; D009068:Movement; D009119:Muscle Contraction; D009154:Mutation; D010058:Oviposition; D016415:Sequence Alignment; D017386:Sequence Homology, Amino Acid
D017931:DNA Primers; D001115:Arecoline; D019204:GTP-Binding Proteins