High impact information on egl-15

• Like egl-15 and sem-5, the other two genes may similarly act in FGFR signaling pathways in C. elegans [1].
• Here we show that egl-15 encodes a receptor tyrosine kinase of the fibroblast growth factor receptor (FGFR) subfamily with multiple roles in development [1].
• Mutations in egl-15 alter the nature of the interaction between the gonad and the SMs, resulting in the posterior displacement of the SMs [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].
• Moreover, a mosaic analysis of mpk-1, which acts downstream of egl-15, suggests that its suppression of Clr (Soc) function is required in the hypodermis [3].

Biological context of egl-15

• The Clr phenotype of clr-1 mutants is mimicked by activation of the EGL-15 fibroblast growth factor receptor (FGFR) and is suppressed by mutations that reduce or eliminate the activity of egl-15 [4].
• To determine the cellular focus of EGL-15 signaling, we identified an enhancer element (e15) within the egl-15 promoter, which is both necessary for the promoter activity and sufficient when duplicated to drive either egl-15 or clr-1 rescue activity [3].
• We identified alternative-splicing defective-1 (asd-1), encoding a new RNA-binding protein of the evolutionarily conserved Fox-1 family, as a regulator of the egl-15 reporter [5].
• Reporters for egl-15 exons 5A and 5B showed tissue-specific profiles, and we isolated mutants defective in the tissue specificity [5].

Anatomical context of egl-15

• 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) [2].

Other interactions of egl-15

• Finally, we have also investigated genetic interactions between let-60 ras and other genes important for sex myoblast migration, including egl-15, which encodes a fibroblast growth factor receptor tyrosine kinase (D. L. DeVore, H. R. Horvitz and M. J. Stern (1995) Cell 83, 611-623) [6].
• 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 [7].

Analytical, diagnostic and therapeutic context of egl-15

• Consistent with this finding, immunofluorescence studies of EGL-15 indicate that EGL-15 is expressed in hypodermal cells, and hypodermal promoters can drive full clr-1 and egl-15 rescue activity [3].

References