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Gene Review:

egl-17 - Protein EGL-17

Caenorhabditis elegans

Burdine, R.D. et al., Kirouac, M. et al., Szewczyk, N.J. et al., Cui, M. et al., Popovici, C. et al., et al.

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High impact information on egl-17

This activation is not suppressed by mutation in either of the known genes encoding FGF ligands (egl-17 or let-756) but is well suppressed when both are mutated, indicating that either ligand is sufficient and at least one is necessary for FGFR activation [1].
While mutations in egl-17 affect only SM migration, mutations in egl-15 can result in larval arrest, scrawny body morphology, and the ability to suppress mutations in clr-1 [2].
egl-17 encodes an invertebrate fibroblast growth factor family member required specifically for sex myoblast migration in Caenorhabditis elegans [2].
Here we clone egl-17 and show it to be a member of the fibroblast growth factor (FGF) family, one of the first functional invertebrate FGFs known. egl-17 shares homology with other FGF members, conserving the key residues required to form the distinctive tertiary structure common to FGFs [2].
sem-4/spalt and egl-17/FGF have a conserved role in sex myoblast specification and migration in P. pacificus and C. elegans [3].

Biological context of egl-17

Since expression of egl-17::GFP driven by the distal enhancer can no longer be turned off at late stages in lin-1 and lin-31 mutants, egl-17 may also be regulated by Ras signaling through repression of LIN-1 and LIN-31 activities [4].

Anatomical context of egl-17

This pattern of vulval cell types is likely to depend on the cis-regulatory regions of the transcriptional targets of intercellular signals in vulval development. egl-17, zmp-1, and cdh-3 are expressed differentially in the developing vulva cells, providing a potential readout for different signaling pathways [5].

Other interactions of egl-17

Here we show that mutations in either of two genes, egl-15 and egl-17, cause the premature termination of the migrations of the SMs [6].
In non-vertebrates, six FGF genes have been identified in Ciona intestinalis, three in Drosophila melanogaster, and two (let-756 and egl-17) in Caenorhabditis elegans [7].
These regions of similarity in C. elegans and C. briggsae upstream of egl-17, zmp-1, and cdh-3 promote expression in vulval cells and the anchor cell (AC) [5].

References

Activated EGL-15 FGF receptor promotes protein degradation in muscles of Caenorhabditis elegans. Szewczyk, N.J., Jacobson, L.A. EMBO J. (2003) [Pubmed]
egl-17 encodes an invertebrate fibroblast growth factor family member required specifically for sex myoblast migration in Caenorhabditis elegans. Burdine, R.D., Chen, E.B., Kwok, S.F., Stern, M.J. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
sem-4/spalt and egl-17/FGF have a conserved role in sex myoblast specification and migration in P. pacificus and C. elegans. Photos, A., Gutierrez, A., Sommer, R.J. Dev. Biol. (2006) [Pubmed]
Cis regulatory requirements for vulval cell-specific expression of the Caenorhabditis elegans fibroblast growth factor gene egl-17. Cui, M., Han, M. Dev. Biol. (2003) [Pubmed]
cis-Regulatory control of three cell fate-specific genes in vulval organogenesis of Caenorhabditis elegans and C. briggsae. Kirouac, M., Sternberg, P.W. Dev. Biol. (2003) [Pubmed]
A normally attractive cell interaction is repulsive in two C. elegans mesodermal cell migration mutants. Stern, M.J., Horvitz, H.R. Development (1991) [Pubmed]
Functional phylogeny relates LET-756 to fibroblast growth factor 9. Popovici, C., Conchonaud, F., Birnbaum, D., Roubin, R. J. Biol. Chem. (2004) [Pubmed]

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