Auditory transduction is mediated by chordotonal (Cho) neurons in Drosophila larvae, but the molecular identity of the mechanotransduction (MET) channel is elusive. Here, we established a whole-cell recording system of Cho neurons and showed that two transient receptor potential vanilloid (TRPV) channels, Nanchung (NAN) and Inactive (IAV), are essential for MET currents in Cho neurons. NAN and IAV form active ion channels when expressed simultaneously in S2 cells. Point mutations in the pore region of NAN-IAV change the reversal potential of the MET currents. Particularly, residues 857 through 990 in the IAV carboxyl terminus regulate the kinetics of MET currents in Cho neurons. In addition, TRPN channel NompC contributes to the adaptation of auditory transduction currents independent of its ion-conduction function. These results indicate that NAN-IAV, rather than NompC, functions as essential pore-forming subunits of the native auditory transduction channel in Drosophila and provide insights into the gating mechanism of MET currents in Cho neurons.

听觉转导由果蝇中的脊索 (Cho) 神经元介导幼虫，但机械转导（MET）通道的分子身份难以捉摸。在这里，我们建立了 Cho 神经元的全细胞记录系统，并表明两个瞬时受体电位香草 (TRPV) 通道，南中 (NAN) 和非活动 (IAV)，对于 Cho 神经元中的 MET 电流是必不可少的。NAN 和 IAV 在 S2 细胞中同时表达时形成活性离子通道。NAN-IAV 孔隙区域的点突变改变了 MET 电流的反转电位。特别是，IAV 羧基末端的 857 到 990 位残基调节 Cho 神经元中 MET 电流的动力学。此外，TRPN 通道 NompC 有助于独立于其离子传导功能的听觉转导电流的适应。这些结果表明，NAN-IAV，而不是 NompC，果蝇并提供对 Cho 神经元中 MET 电流门控机制的见解。