-
- Richard G. Walker
- Departments of Biology and Neurosciences and
-
- Aarron T. Willingham
- Departments of Biology and Neurosciences and
-
- Charles S. Zuker
- Howard Hughes Medical Institute, University of California, San Diego, La Jolla, CA 92093–0649, USA.
抄録
<jats:p> Mechanosensory transduction underlies a wide range of senses, including proprioception, touch, balance, and hearing. The pivotal element of these senses is a mechanically gated ion channel that transduces sound, pressure, or movement into changes in excitability of specialized sensory cells. Despite the prevalence of mechanosensory systems, little is known about the molecular nature of the transduction channels. To identify such a channel, we analyzed <jats:italic>Drosophila melanogaster</jats:italic> mechanoreceptive mutants for defects in mechanosensory physiology. Loss-of-function mutations in the <jats:italic>no mechanoreceptor potential C</jats:italic> ( <jats:italic>nompC</jats:italic> ) gene virtually abolished mechanosensory signaling. <jats:italic>nompC</jats:italic> encodes a new ion channel that is essential for mechanosensory transduction. As expected for a transduction channel, <jats:italic>D. melanogaster</jats:italic> NOMPC and a <jats:italic>Caenorhabditis elegans</jats:italic> homolog were selectively expressed in mechanosensory organs. </jats:p>
収録刊行物
-
- Science
-
Science 287 (5461), 2229-2234, 2000-03-24
American Association for the Advancement of Science (AAAS)
- Tweet
キーワード
詳細情報
-
- CRID
- 1364233268469492352
-
- NII論文ID
- 80011719112
-
- ISSN
- 10959203
- 00368075
-
- データソース種別
-
- Crossref
- CiNii Articles