MEC-10 and MEC-19 reduce the neurotoxicity of the MEC-4(d) DEG/ENaC channel in Caenorhabditis elegans

Yushu Chen, Shashank Bharill, Robert O'Hagan, Ehud Y. Isacoff, Martin Chalfie

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

The Caenorhabditis elegans DEG/ENaC proteins MEC-4 and MEC-10 transduce gentle touch in the six touch receptor neurons . Gain-of-function mutations of mec-4 and mec-4(d) result in a hyperactive channel and neurodegeneration in vivo. Loss of MEC-6, a putative DEG/ENaC-specific chaperone, and of the similar protein POML-1 suppresses the neurodegeneration caused by a mec-4(d) mutation. We find that mutation of two genes, mec-10 and a new gene mec-19 (previously named C49G9.1), prevents this action of POML-1, allowing the touch receptor neurons to die in poml-1 mec-4(d) animals. The proteins encoded by these genes normally inhibit mec-4(d) neurotoxicity through different mechanisms. MEC-10, a subunit of the mechanosensory transduction channel with MEC-4, inhibits MEC-4(d) activity without affecting MEC-4 expression. In contrast, MEC-19, a membrane protein specific to nematodes, inhibits MEC-4(d) activity and reduces MEC-4 surface expression.

Original languageEnglish
Pages (from-to)1121-1130
Number of pages10
JournalG3: Genes, Genomes, Genetics
Volume6
Issue number4
DOIs
StatePublished - 1 Jan 2016

Keywords

  • Caenorhabditis elegans
  • DEG/ENaC channels
  • Neurodegeneration
  • Physiological suppressors
  • Touch sensitivity

Fingerprint Dive into the research topics of 'MEC-10 and MEC-19 reduce the neurotoxicity of the MEC-4(d) DEG/ENaC channel in Caenorhabditis elegans'. Together they form a unique fingerprint.

  • Cite this