MEC-2 regulates C. elegans DEG/ENaC channels needed for mechanosensation
作者： Miriam B. Goodman , Glen G. Ernstrom , Dattananda S. Chelur , Robert O'Hagan , C. Andrea Yao
DOI: 10.1038/4151039A
关键词: Ion channel 、 Cell biology 、 Mechanosensation 、 Caenorhabditis elegans 、 Stomatin 、 Anatomy 、 Acid-sensing ion channel 、 Electrophysiology 、 Degenerin Sodium Channels 、 Biology 、 Stretch-activated ion channel 、 Multidisciplinary
摘要: Touch sensitivity in animals relies on nerve endings the skin that convert mechanical force into electrical signals. In nematode Caenorhabditis elegans, gentle touch to body wall is sensed by six mechanosensory neurons express two amiloride-sensitive Na+ channel proteins (DEG/ENaC). These proteins, MEC-4 and MEC-10, are required for sensation can mutate cause neuronal degeneration. Here we show these mutant or 'd' forms of MEC-10 produce a constitutively active, ionic current when co-expressed Xenopus oocytes, but not their own. MEC-2, stomatin-related protein needed sensitivity, increased activity channels about 40-fold allowed currents be detected with wild-type MEC-10. Whereas neither central, stomatin-like domain MEC-2 nor human stomatin retained full-length both produced MEC-4d. Our findings indicate regulates MEC-4/MEC-10 ion raise possibility similar may formed DEG/ENaC vertebrates invertebrates. Some mediate responses.
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