ZFIN ID: ZDB-PUB-030715-6
NompC TRP channel required for vertebrate sensory hair cell mechanotransduction
Sidi, S., Friedrich, R.W., and Nicolson, T.
Date: 2003
Source: Science (New York, N.Y.)   301(5629): 96-99 (Journal)
Registered Authors: Friedrich, Rainer, Nicolson, Teresa, Sidi, Samuel
Keywords: none
MeSH Terms:
  • Amino Acid Sequence
  • Animals
  • Cochlear Microphonic Potentials
  • Computational Biology
  • Deafness
  • Ear, Inner/embryology
  • Endocytosis
  • Gene Expression
  • Hair Cells, Auditory/physiology*
  • Hearing
  • In Situ Hybridization
  • Ion Channels/chemistry
  • Ion Channels/genetics
  • Ion Channels/physiology*
  • Mechanotransduction, Cellular*
  • Molecular Sequence Data
  • Oligonucleotides, Antisense
  • Phenotype
  • Phylogeny
  • Postural Balance
  • Reflex, Startle
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transient Receptor Potential Channels
  • Zebrafish
  • Zebrafish Proteins/chemistry
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/physiology*
PubMed: 12805553 Full text @ Science
The senses of hearing and balance in vertebrates rely on the sensory hair cells (HCs) of the inner ear. The central element of the HC's transduction apparatus is a mechanically gated ion channel of unknown identity. Here we report that the zebrafish ortholog of Drosophila no mechanoreceptor potential C (nompC), which encodes a transient receptor potential (TRP) channel, is critical for HC mechanotransduction. In zebrafish larvae, nompC is selectively expressed in sensory HCs. Morpholino-mediated removal of nompC function eliminated transduction-dependent endocytosis and electrical responses in HCs, resulting in larval deafness and imbalance. These observations indicate that nompC encodes a vertebrate HC mechanotransduction channel.