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Published May 1996 | public
Journal Article Open

Mutations in a C. elegans G_qα Gene Disrupt Movement, Egg Laying, and Viability


We find that C. elegans egl-30 encodes a heterotrimeric G protein α subunit more than 80% identical to mammalian G_qα family proteins, and which can function as a G_qα 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 G_qα 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.

Additional Information

© 1996 Cell Press. Received 6 November 1995, Revised 22 March 1996. We thank Harry Duttweiler, who selected and partially backcrossed the eat-11 suppressors, and Steve Marsh and Rick Colayco (Caltech DNA sequencing core facility) for assistance in determining the egl-30 lesions. The C. elegans Genetic Stock Center provided some of the strains described here. This work was funded by a grant from the Human Frontiers in Science Organization to M. I. S and P. W. S., research grant HL46154 from the United States Public Health Service to L. A., and National Research Service Award F32NS09541–03 to L. B. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC Section 1734 solely to indicate this fact.

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August 20, 2023
August 20, 2023