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Significance Auditory hair cells receive olivocochlear efferent innervation, which improves sound discrimination and mitigates acoustic trauma. The olivocochlear synapse involves α9α10 nicotinic acetylcholine receptors (nAChRs), which do not express in recombinant cell lines. Here, genome-wide screening determined that assembly and surface expression of α9α10 require ligand binding. Ion channel function additionally demands an auxiliary subunit, which can be transmembrane inner ear (TMIE) or TMEM132e. These single-pass transmembrane proteins are enriched in hair cells and underlie nonsyndromic human deafness. Inner hair cells from TMIE mutant mice show altered postsynaptic α9α10 function and abnormally retain α9α10-mediated transmission through development. This study identifies unexpected functions for human deafness genes TMIE/TMEM132e and enables drug discovery for this elusive nAChR implicated in prevalent auditory disorders.

Hair cell α9α10 nicotinic acetylcholine receptor functional expression regulated by ligand binding and deafness gene products