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Resources » Paper

Itay, Nakdimon et al. (2010) C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany "Cross talk between the Ras-MAPK and Insulin pathways during vulval development"

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00036875

    Itay, Nakdimon, & Hajnal, Alex (2010). Cross talk between the Ras-MAPK and Insulin pathways during vulval development presented in C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany. Unpublished information; cite only with author permission.

    The development of the vulva, the egg-laying organ of the hermaphrodite, serves as an excellent model to study how inter- and intracellular signals control cell fate specification and pattern formation during organogenesis. Previous work from our lab showed that a InsR/daf-2 reduction-of-function (rf) mutation reduces the Multivulva (Muv) phenotype of a let-60 gain-of-function (gf) allele (Battu et al. 2003). Further epistasis analysis showed that although loss of PI3K/age-1 function (lf) only partially suppresses the let-60(gf) Muv phenotype, PTEN/daf-18(lf) significantly increased the number of VPCs induced in a let-60(gf) background independently of AKT-1/-2 and DAF-16 function. Moreover, a mutated DAF-18(G174E) rescue construct that can dephosphorylate proteins but not lipids only showed a weak rescue, suggesting that elevated P IP3 levels enhance RAS/MAPK-induced vulval development and that an alternative PI3K might function besides AGE-1. daf-18(lf) partially suppressed the Vulvaless (Vul) phenotype of mutants in other RAS/MAPK pathway components such as lin-2(lf), let-23(rf), sos-1(lf) and lin-45(rf), but failed to suppress mpk-1(lf) mutants. These results suggest that elevated PIP3 levels in daf-18(lf) activate the RAS/MAPK pathway downstream of or in parallel with SOS-1 and upstream of or at the level of MPK-1. A rescuing translational DAF-18::GFP reporter showed strong membrane expression in all induced VPCs, the uterus, the spermatheca and the ventral nerve cord. In conclusion, we have shown that PIP3 levels, which are regulated by Insulin signaling and DAF-18, modulate RAS/MAPK signaling in the VPCs.


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