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Gene Review

sem-5  -  Protein SEM-5

Caenorhabditis elegans

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High impact information on sem-5

  • Like egl-15 and sem-5, the other two genes may similarly act in FGFR signaling pathways in C. elegans [1].
  • One of these genes, sem-5, encodes an adaptor molecule that transduces signals from a variety of receptor tyrosine kinases [1].
  • We report here the identification and characterization of a new gene, sem-5 (sem, sex muscle abnormal), that acts both in vulval induction and in sex myoblast migration [2].
  • On the basis of its DNA sequence, sem-5 encodes a novel 228-amino-acid protein which consists almost entirely of one SH2 (SH, src homology region) and two SH3 domains [2].
  • Moreover, ptp-2(op194) increased the penetrance of the vulvaless phenotype conferred by a weak loss-of-function sem-5 allele [3].

Biological context of sem-5


Anatomical context of sem-5

  • Mutations in sem-5 confer dramatic sex myoblast positioning defects in double mutant combinations with unc-53, unc-71, or unc-73 mutations, even in the presence of the gonad [7].


  1. An FGF receptor signaling pathway is required for the normal cell migrations of the sex myoblasts in C. elegans hermaphrodites. DeVore, D.L., Horvitz, H.R., Stern, M.J. Cell (1995) [Pubmed]
  2. C. elegans cell-signalling gene sem-5 encodes a protein with SH2 and SH3 domains. Clark, S.G., Stern, M.J., Horvitz, H.R. Nature (1992) [Pubmed]
  3. The Caenorhabditis elegans SH2 domain-containing protein tyrosine phosphatase PTP-2 participates in signal transduction during oogenesis and vulval development. Gutch, M.J., Flint, A.J., Keller, J., Tonks, N.K., Hengartner, M.O. Genes Dev. (1998) [Pubmed]
  4. ARK-1 inhibits EGFR signaling in C. elegans. Hopper, N.A., Lee, J., Sternberg, P.W. Mol. Cell (2000) [Pubmed]
  5. The human GRB2 and Drosophila Drk genes can functionally replace the Caenorhabditis elegans cell signaling gene sem-5. Stern, M.J., Marengere, L.E., Daly, R.J., Lowenstein, E.J., Kokel, M., Batzer, A., Olivier, P., Pawson, T., Schlessinger, J. Mol. Biol. Cell (1993) [Pubmed]
  6. Introduction of a loss-of-function point mutation from the SH3 region of the Caenorhabditis elegans sem-5 gene activates the transforming ability of c-abl in vivo and abolishes binding of proline-rich ligands in vitro. Van Etten, R.A., Debnath, J., Zhou, H., Casasnovas, J.M. Oncogene (1995) [Pubmed]
  7. Genetic enhancers of sem-5 define components of the gonad-independent guidance mechanism controlling sex myoblast migration in Caenorhabditis elegans hermaphrodites. Chen, E.B., Branda, C.S., Stern, M.J. Dev. Biol. (1997) [Pubmed]
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