#  Transgenic Tmc2 expression preserves inner ear hair cells and vestibular function in mice lacking Tmc1 

 





August 14, 2018

 

 

Recent work has demonstrated that transmembrane channel-like 1 protein (TMC1) is an essential component of the sensory transduction complex in hair cells of the inner ear. A closely related homolog, TMC2, is expressed transiently in the neonatal mouse cochlea and can enable sensory transduction in *Tmc1*-null mice during the first postnatal week. Both TMC1 and TMC2 are expressed at adult stages in mouse vestibular hair cells. The extent to which TMC1 and TMC2 can substitute for each other is unknown. Several biophysical differences between TMC1 and TMC2 suggest these proteins perform similar but not identical functions. To investigate these differences, and whether TMC2 can substitute for TMC1 in mature hair cells, we generated a knock-in mouse model allowing *Cre*-inducible expression of *Tmc2*. We assayed for changes in hair cell sensory transduction and auditory and vestibular function in *Tmc2* knockin mice (*Tm*[*Tmc2*]) in the presence or absence of endogenous *Tmc1*, *Tmc2* or both. Our results show that expression of Tm[TMC2] restores sensory transduction in vestibular hair cells and transiently in cochlear hair cells in the absence of TMC1. The cellular rescue leads to recovery of balance but not auditory function. We conclude that TMC1 provides some additional necessary function, not provided by TMC2. [Read more.](https://www.nature.com/articles/s41598-018-28958-x)

 

 

 



 

 

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