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.