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Resources » Paper

Kapelle, William et al. (2010) C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany "Hyper-activation of Notch signaling can rescue proliferation in meg-1 mutants"

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  • Comments on Kapelle, William et al. (2010) C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany "Hyper-activation of Notch signaling can rescue proliferation in meg-1 mutants" (0)

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00036884

    Kapelle, William, & Reinke, Valerie (2010). Hyper-activation of Notch signaling can rescue proliferation in meg-1 mutants presented in C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany. Unpublished information; cite only with author permission.

    P granules are present continually in the germ line of C. elegans at all stages of development. MEG-1 and MEG-2 are unique in that they localize exclusively to embryonic P granules during a brief developmental stage when the germ lineage is being separated from the soma. meg-1 mutants however, have only a minor embryonic phenotype, while in larvae germ cells fail to proliferate, resulting in sterility. To investigate the function of MEG-1 in the early embryo when the germ line is being established, we are conducting an RNAi screen for suppressors and enhancers of meg-1 mutants. A pilot screen has already identified four factors that enhance sterility in meg-1 mutants ( nos-2, pgl-2, T02G5.11 and C37A2.8 ), and two that suppress sterility ( nos-3 and gld-1 ). GLD-1 is of particular interest for the role it pla ys in repressing GLP-1(Notch) signaling in the gonad to inhibit proliferation. We therefore tested whether downregulation of Notch signaling (presumably by GLD-1) was critical for the meg-1 phenotype and found that constitutive activation of Notch via the glp-1(oz112gf) mutant was able to partially suppress the meg-1 proliferation defect. These results indicate that meg-1 mutant germ cells are indeed competent for proliferation if Notch signaling in the gonad fails to be downregulated. Interestingly, the over-proliferation defect of glp-1(oz112gf) was also somewhat suppressed by loss of meg-1 activity, which implies that meg-1 is required to render germ cells sensitive to Notch signaling, suggesting that these two pathways strike a balance to control proliferation in the C. elegans germ line. Additionally, the screen has the potential to identify other factors that genetically interact with meg-1 .


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