TMC1 and TMC2 are components of the mechanotransduction channel in hair cells of the mammalian inner ear.

Neuron

Department of Otolaryngology, F.M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Center for Life Sciences 12251, Boston, MA 02115, USA.

Published: August 2013

AI Article Synopsis

  • TMC1 and TMC2 genes are essential for sensory transduction in auditory and vestibular hair cells, but their specific functions were previously unclear.
  • Research found that cells with TMC2 showed high calcium permeability and larger currents, while those with a mutant form of TMC1 exhibited reduced calcium permeability and currents.
  • The findings indicate that TMC1 and TMC2 are critical components of ion channels in hair cells and may influence how sensory transduction varies across different parts of the cochlea.

Article Abstract

Sensory transduction in auditory and vestibular hair cells requires expression of transmembrane channel-like (Tmc) 1 and 2 genes, but the function of these genes is unknown. To investigate the hypothesis that TMC1 and TMC2 proteins are components of the mechanosensitive ion channels that convert mechanical information into electrical signals, we recorded whole-cell and single-channel currents from mouse hair cells that expressed Tmc1, Tmc2, or mutant Tmc1. Cells that expressed Tmc2 had high calcium permeability and large single-channel currents, while cells with mutant Tmc1 had reduced calcium permeability and reduced single-channel currents. Cells that expressed Tmc1 and Tmc2 had a broad range of single-channel currents, suggesting multiple heteromeric assemblies of TMC subunits. The data demonstrate TMC1 and TMC2 are components of hair cell transduction channels and contribute to permeation properties. Gradients in TMC channel composition may also contribute to variation in sensory transduction along the tonotopic axis of the mammalian cochlea.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3827726PMC
http://dx.doi.org/10.1016/j.neuron.2013.06.019DOI Listing

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