Mutations in a C. elegans Gqα Gene Disrupt Movement, Egg Laying, and Viability
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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.
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egl-30 loss-of-function mutants have a straight posture and are almost immobile on food.
“In C. elegans, loss-of-function mutants in the trimeric G-protein Gαq (encoded by egl-30) have a straight posture and are almost immobile on food”
From Two Rab2 Interactors Regulate Dense-Core Vesicle Maturation (2014) · cites this paper as Brundage et al., 1996
The movement results (p. 5) report that egl-30 mutants moved less, and that ad805 and n715 animals were almost paralyzed when undisturbed on an E. coli lawn. But the other strains were described as sluggish rather than almost immobile. The paper reports shallow or flattened movement tracks and flaccidity, not a straight posture for all loss-of-function mutants. (LLM, conf=0.84)
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- Authors
- Brundage, L., Avery, L., Katz, A., Kim, U.-J., Mendel, J. E., Sternberg, P. W., & Simon, M. I.
- Affiliations
- California Institute of Technology (US)
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Simon, Melvin I
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 1996-05
- Volume
- 16
- Issue
- 5
- Pages
- 999-1009
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC4444781
- OpenAlex
- W2009821005
- Cited by
- 195
- References
- 53
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 2 · 2023: 4 · 2022: 5 · 2021: 5 · 2020: 6 · 2019: 1 · 2018: 7 · 2017: 10 · 2016: 5 · 2015: 2 · 2014: 6 · 2013: 13 · 2012: 3
- FWCI
- 2.65
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R37HL046154, HL46154, R01HL046154)
- National Institute of Neurological Disorders and Stroke (F32NS09541-03, F32NS009541)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurobiology and Insect Physiology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- egl-30, Gαq, heterotrimeric G proteins, Caenorhabditis elegans, acetylcholine response, oviposition, locomotion, neuromuscular junction, muscle defects, early termination, gene overexpression, mutant allele, viability
- MeSH terms
- Amino Acid Sequence, Animals, Arecoline, Base Sequence, Female, Molecular Sequence Data, Movement, Muscle Contraction, Mutation, Oviposition, Sequence Alignment, Caenorhabditis elegans, Sequence Homology, Amino Acid, DNA Primers, GTP-Binding Proteins
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