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TY - JOUR AU - Goodman, Miriam B. AU - Ernstrom, Glen G. AU - Chelur, Dattananda S. AU - O'Hagan, Robert AU - Yao, C. Andrea AU - Chalfie, Martin PY - 2002 DA - 2002/02/01 TI - MEC-2 regulates C. elegans DEG/ENaC channels needed for mechanosensation JO - Nature SP - 1039 EP - 1042 VL - 415 IS - 6875 AB - Touch sensitivity in animals relies on nerve endings in the skin that convert mechanical force into electrical signals. In the nematode Caenorhabditis elegans, gentle touch to the body wall is sensed by six mechanosensory neurons1 that express two amiloride-sensitive Na+ channel proteins (DEG/ENaC). These proteins, MEC-4 and MEC-10, are required for touch sensation and can mutate to cause neuronal degeneration2,3. Here we show that these mutant or ‘d’ forms of MEC-4 and MEC-10 produce a constitutively active, amiloride-sensitive ionic current when co-expressed in Xenopus oocytes, but not on their own. MEC-2, a stomatin-related protein needed for touch sensitivity4, increased the activity of mutant channels about 40-fold and allowed currents to be detected with wild-type MEC-4 and MEC-10. Whereas neither the central, stomatin-like domain of MEC-2 nor human stomatin retained the activity of full-length MEC-2, both produced amiloride-sensitive currents with MEC-4d. Our findings indicate that MEC-2 regulates MEC-4/MEC-10 ion channels and raise the possibility that similar ion channels may be formed by stomatin-like proteins and DEG/ENaC proteins that are co-expressed in both vertebrates and invertebrates5,6,7,8. Some of these channels may mediate mechanosensory responses. SN - 1476-4687 UR - https://doi.org/10.1038/4151039a DO - 10.1038/4151039a ID - Goodman2002 ER -