mec-15 encodes an F-box protein required for touch receptor neuron mechanosensation, synapse formation and development

Alexander Bounoutas, Qun Zheng, Michael L. Nonet, Martin Chalfie

Research output: Contribution to journalArticle

23 Scopus citations

Abstract

Selective protein degradation is a key regulator of neuronal development and synaptogenesis. Complexes that target proteins for degradation often contain F-box proteins. Here we characterize MEC-15, an F-box protein with WD repeats, which is required for the development and function of Caenorhabditis elegans touch receptor neurons (TRNs). Mutations in mec-15 produce defects in TRN touch sensitivity, chemical synapse formation, and cell-body morphology. All mec-15 mutant phenotypes are enhanced by mutations in a MAP kinase pathway composed of the MAPKKK DLK-1, the MAPKK MKK-4, and the p38 MAPK PMK-3. A mutation of the rpm-1 gene, which encodes an E3 ubiquitin ligase that negatively regulates this pathway to promote synaptogenesis, suppresses only the mec-15 cell-body defect. Thus, MEC-15 acts in parallel with RPM-1, implicating a second protein degradation pathway in TRN development. In addition, all mec-15 phenotypes can be dominantly suppressed by mutations in mec-7, which encodes a β-tubulin, and dominantly enhanced by mutations in mec-12, which encodes an α-tubulin. Since mec-15 phenotypes depend on the relative levels of these tubulins, MEC-15 may target proteins whose function is affected by these levels.

Original languageEnglish
Pages (from-to)607-617
Number of pages11
JournalGenetics
Volume183
Issue number2
DOIs
StatePublished - 2009

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