Two Caenorhabditis elegans genes,
unc-8 and
sup-40, have been newly identified, by genetic criteria, as regulating ion channel function in motorneurons. Two dominant
unc-8 alleles cause motorneuron swelling similar to that of other neuronal types in dominant mutants of the
deg-1 gene family, which is homologous to a mammalian gene family encoding amiloride-sensitive sodium channel subunits. As for previously identified
deg-1 family members,
unc-8 dominant mutations are recessively suppressed by mutations in the
mec-6 gene, which probably encodes a second type of channel component. An unusual dominant mutation,
sup-41 (
lb125), also co-suppresses
unc-8 and
deg-1, suggesting the existence of yet another common component of ion channels containing
unc-8 or
deg-1 subunits. Dominant, transacting, intragenic suppressor mutations have been isolated for both
unc-8 and
deg-1, consistent with the idea that, like their mammalian homologues, the two gene products function as multimers. The
sup-40 (
lb130) mutation dominantly suppresses
unc-8 motorneuron swelling and produces a novel swelling phenotype in hypodermal nuclei.
sup-40 may encode an ion channel component or regulator that can correct the osmotic defect caused by abnormal
unc-8 channels.