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Caenorhabditis elegans SOS-1 is necessary for multiple RAS-mediated developmental signals.

The EMBO journal | Jul 3, 2000

http://www.ncbi.nlm.nih.gov/pubmed/10880441

Vulval induction in Caenorhabditis elegans has helped define an evolutionarily conserved signal transduction pathway from receptor tyrosine kinases (RTKs) through the adaptor protein SEM-5 to RAS. One component present in other organisms, a guanine nucleotide exchange factor for Ras, has been missing in C.ELEGANS: To understand the regulation of this pathway it is crucial to have all positive-acting components in hand. Here we describe the identification, cloning and genetic characterization of C.ELEGANS: SOS-1, a putative guanine nucleotide exchanger for LET-60 RAS. RNA interference experiments suggest that SOS-1 participates in RAS-dependent signaling events downstream of LET-23 EGFR, EGL-15 FGFR and an unknown RTK. We demonstrate that the previously identified let-341 gene encodes SOS-1. Analyzing vulval development in a let-341 null mutant, we find an SOS-1-independent pathway involved in the activation of RAS signaling. This SOS-1-independent signaling is not inhibited by SLI-1/Cbl and is not mediated by PTP-2/SHP, raising the possibility that there could be another RasGEF.

Pubmed ID: 10880441 RIS Download

Mesh terms: Alleles | Amino Acid Sequence | Animals | Base Sequence | Caenorhabditis elegans | DNA Primers | Female | GTPase-Activating Proteins | Ligands | Molecular Sequence Data | Phenotype | RNA, Double-Stranded | Receptors, Fibroblast Growth Factor | SOS1 Protein | Sequence Homology, Amino Acid | Signal Transduction | Vulva | ras Proteins

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Associated grants

  • Agency: NIGMS NIH HHS, Id: GM07616
  • Agency: NICHD NIH HHS, Id: HD23690

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