Differential functions of the C. elegans FGF receptor in axon outgrowth and maintenance of axon position

Hannes E. Bülow, Thomas Boulin, Oliver Hobert

Research output: Contribution to journalArticle

74 Scopus citations

Abstract

Wiring of the nervous system requires that axons navigate to their targets and maintain their correct positions in axon fascicles after termination of axon outgrowth. We show here that the C. elegans fibroblast growth factor receptor (FGFR), EGL-15, affects both processes in fundamentally distinct manners. FGF-dependent activation of the EGL-15 tyrosine kinase and subsequently the GTPase LET-60/ras is required within epidermal cells, the substratum for most outgrowing axon, for appropriate outgrowth of specific axon classes to their target area. In contrast, genetic elimination of the FGFR isoform EGL-15(5A), defined by the inclusion of an alternative extracellular interimmunoglobulin domain, has no consequence for axon outgrowth but leads to a failure to postembryonically maintain axon position within defined axon fascicles. An engineered, secreted form of EGL-15(5A) containing only its ectodomain is sufficient for maintenance of axon position, thus providing novel insights into receptor tyrosine kinase function and the process of maintaining axon position.

Original languageEnglish (US)
Pages (from-to)367-374
Number of pages8
JournalNeuron
Volume42
Issue number3
DOIs
StatePublished - May 13 2004
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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