Mechanosensory transduction underlies a wide range of senses, including pro
prioception, touch, balance, and hearing. The pivotal element of these sens
es 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 molecu
lar nature of the transduction channels. To identify such a channel, we ana
lyzed Drosophila melanogaster mechanoreceptive mutants for defects in mecha
nosensory physiology, Loss-of-function mutations in the no mechanoreceptor
potential C (nompC) gene virtually abolished mechanosensory signaling. nomp
C encodes a new ion channel that is essential for mechanosensory transducti
on. As expected for a transduction channel, D, melanogaster NOMPC and a Cae
norhabditis elegans homolog were selectively expressed in mechanosensory or
gans.