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Resources » Paper

Sternberg PW et al. (2000) West Coast Worm Meeting "Characterization and Suppression of eat-16; sag-1/dgk-1 lethality"

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  • Comments on Sternberg PW et al. (2000) West Coast Worm Meeting "Characterization and Suppression of eat-16; sag-1/dgk-1 lethality" (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00016916

    Sternberg PW, Hajdu-Cronin YM, & Chen WJ (2000). Characterization and Suppression of eat-16; sag-1/dgk-1 lethality presented in West Coast Worm Meeting. Unpublished information; cite only with author permission.

    goa-1 (Gao) modulates many behaviors in C. elegans, including locomotion, egg-laying, and feeding. Reducing function in goa-1 causes hyperactive locomotion and constitutive egg laying (1, 2); in contrast, overexpressing the constitutively activated Q205L mutation causes lethargy and cessation of egg laying (1). Previously, we screened for suppressors of the paralysis of syIs17, an integrated transgene containing goa-1(Q205L) under control of a heat shock promoter. Hyperactive mutants were isolated in two genes, eat-16 and sag-1/dgk-1. We found that in addition to suppressing the phenotype of activated Gao, eat-16 and sag-1/dgk-1 mutations also partially suppressed the phenotype of several reduction of function mutations in egl-30 ( C. elegans Gaq). eat-16 encodes a regulator of G protein signaling, which we believe functions as a GAP for EGL-30, and sag-1/dgk-1 encodes a diacyl glycerol kinase (3) which likely functions to reduce the levels of diacyl glycerol (DAG), a second messenger produced upon stimulation of PLCb by activated EGL-30. eat-16(sy438) and sag-1/dgk-1(sy428) double mutants arrest during larval development. This lethal phenotype is highly penetrant (>99%). We hypothesized that the lethality of eat-16; sag-1/dgk-1 is caused by excessive levels of second messengers produced downstream of Gaq, such as DAG. In support of this hypothesis, the triple mutant egl-30(md186) eat-16(sy438); sag-1/dgk-1(sy428) is viable to adulthood and fertile. To further understand the cause of death and identify more components in the pathway, we are seeking other suppressors of eat-16; sag/dgk-1 lethality besides egl-30, both by testing mutations in genes that have already been described, and by screening for new suppressors. To date we have screened about 7000 genomes and have backcrossed 7 suppressor mutants. We are beginning to characterize the lethal phenotype by Nomarski optics and plan to determine the site of action. References: Mendel et al., 1995. Science 267: 1652-1655. Segalat et al., 1995. Science 267: 1648-1651. Nurrish et al., 1999. Neuron 24: 231-242


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