egl-17 encodes an invertebrate fibroblast growth factor family member required specifically for sex myoblast migration in Caenorhabditis elegans

egl-17 encodes an invertebrate fibroblast growth factor family member required specifically for sex myoblast migration in Caenorhabditis elegans

Departments of ^*Cell Biology, ^†Biology, and ^‡Genetics, Yale University, P.O. Box 208005, New Haven, CT 06520-8005

Abstract

The proper guidance of the Caenorhabditis elegans hermaphrodite sex myoblasts (SMs) requires the genes egl-15 and egl-17. egl-15 has been shown to encode the C. elegans orthologue of the fibroblast growth factor receptor (FGFR). 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. Genetic and molecular evidence demonstrates that the SM migration defect seen in egl-17 mutant animals represents complete loss of egl-17 function. 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. We propose that EGL-17 (FGF) acts as a ligand for EGL-15 (FGFR) specifically during SM migration and that another ligand(s) activates EGL-15 for its other functions.

Footnotes

↵ § To whom reprint requests should be addressed. e-mail: Michael_Stern{at}QM.Yale.edu.
H. Horvitz, Massachusetts Institute of Technology, Cambridge, MA
Data deposition: The sequence reported in this paper has been deposited in the GenBank database (accession no. U85766U85766).
ABBREVIATIONS:

FGF,

fibroblast growth factor;

FGFR,

FGF receptor;

SMs,

sex myoblasts, Egl, egg-laying-defective;

RT-PCR,

reverse transcription–PCR;

RACE,

rapid amplification of cDNA ends