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Published July 3, 2000 | public
Journal Article

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

Abstract

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.

Additional Information

© 2000 European Molecular Biology Organization. Received January 20, 2000; revised and accepted May 15, 2000. We thank M. Stern for providing his unpublished let‐341(n2183) and sem‐5(ay73) alleles and for discussion of FGF receptor signaling; Z. Chen and M. Han for their generosity in providing their unpublished let‐341(ku231) allele; and N. Moghal and J. Alberola‐Ila for critical reading of this manuscript. Some strains were provided by the Caenorhabditis Genetics Center, supported by the National Center for Research Resources of the National Institutes of Health. This work has been supported by US Public Health Service grant (HD23690) to P.W.S., an investigator with the Howard Hughes Medical Institute. C.C. is funded by a NIH predoctoral training grant (GM07616).

Additional details

Created:
August 21, 2023
Modified:
October 20, 2023