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

• We find that sem-5 also has a negative function in let-23-mediated ovulation and suggest that this negative function is mediated by the recruitment of inhibitors such as ARK-1 [4].
• Mutations in the Caenorhabditis elegans gene sem-5 affect cell signaling processes involved in guiding a class of cell migrations and inducing vulval cell fates [5].
• 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 [6].
• We have introduced two loss-of-function point mutations from highly conserved regions of the src homology 3 (SH3) domains of the Caenorhabditis elegans sem-5 gene into the SH3 domain of the murine type IV c-abl tyrosine kinase proto-oncogene [6].
• Genetic enhancers of sem-5 define components of the gonad-independent guidance mechanism controlling sex myoblast migration in Caenorhabditis elegans hermaphrodites [7].

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].

References