CLEC-38, a transmembrane protein with C-type lectin-like domains, negatively regulates UNC-40-mediated axon outgrowth and promotes presynaptic development in Caenorhabditis elegans

Gauri Kulkarni, Haichang Li, William G. Wadsworth

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

Abstract

In the developing nervous system, axons respond to various guidance cues to find their targets. The effects guidance cues have on an axon may change as an axon undergoes morphological changes, such as branching, turning, and synapse formation. The means by which these changes are regulated are not well understood. In Caenorhabditis elegans, the UNC-40/DCC (deleted in colorectal cancer) receptor mediates responses to the UNC-6/netrin guidance cue. Here, we show that CLEC-38, a protein with predicted transmembrane and C-type lectin-like domains, regulates UNC-40-mediated axon outgrowth as well as the organization of presynaptic terminals. We observe that, in genetic backgrounds sensitized for axon guidance defects, loss of clec-38 function can suppress defects in an UNC-40-dependent manner. Within migrating axons, clec-38 acts cell autonomously. Furthermore, loss of clec-38 function alters UNC-40::GFP (green fluorescent protein) expression. We also observe that loss of clec-38 function disrupts presynaptic patterning in animals with normal axon guidance and that there are genetic interactions between clec-38 and rpm-1, which encodes a protein implicated in regulating presynaptic assembly and axon morphology. We suggest CLEC-38 plays a role in promoting synapse assembly and refining axon outgrowth activity.

Original languageEnglish (US)
Pages (from-to)4541-4550
Number of pages10
JournalJournal of Neuroscience
Volume28
Issue number17
DOIs
StatePublished - Apr 23 2008

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Keywords

  • Axon guidance
  • C. elegans
  • Development
  • Genetics
  • Growth cone
  • Receptor
  • Synaptogenesis

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