Distinct roles for innexin gap junctions and hemichannels in mechanosensation.

Abstract

Mechanosensation is central to a wide range of functions, including tactile and pain perception, hearing, proprioception, and control of blood pressure, but identifying the molecules underlying mechanotransduction has proved challenging. In <i>Caenorhabditis elegans</i>, the avoidance response to gentle body touch is mediated by six touch receptor neurons (TRNs), and is dependent on MEC-4, a DEG/ENaC channel. We show that hemichannels containing the innexin protein UNC-7 are also essential for gentle touch in the TRNs, as well as harsh touch in both the TRNs and the PVD nociceptors. UNC-7 and MEC-4 do not colocalize, suggesting that their roles in mechanosensory transduction are independent. Heterologous expression of <i>unc-7</i> in touch-insensitive chemosensory neurons confers ectopic touch sensitivity, indicating a specific role for UNC-7 hemichannels in mechanosensation. The <i>unc-7</i> touch defect can be rescued by the homologous mouse gene <i>Panx1</i> gene, thus, innexin/pannexin proteins may play broadly conserved roles in neuronal mechanotransduction.