The mec-2 gene is required for the function of a set of six touch receptor neurons in the nematode Caenorhabditis elegans; mec-2 mutants, which are touch-insensitive, have touch cells that appear morphologically normal^1,2. Gene interaction studies suggest that mec-2 positively regulates the activity of the putative mechano-sensory transduction channel (ref. 3 and the present paper), comprised in part of proteins encoded by the two degenerin genes mec-4 and mec-10 (refs 3–5). The central region of the mec-2 protein (MEC-2) is very similar to stomatin, an integral membrane protein (band 7.2b) in human red blood cells that is thought to regulate cation conductance⁶. MEC-2-LacZ fusions are distributed along the touch receptor axons. This axonal distribution, which is mediated by the mec-2-specific amino terminus, is disrupted by mutations in mec-12, an α-tubulin gene needed for touch cell function. Our results indicate that MEC-2 links the mechanosensory channel and the microtubule cytoskeleton of the touch receptor neurons. Such linkage provides the basis for a mechanism of mechanosensation whereby microtubule displacement leads to channel opening.