Abstract
The nematode C. elegans uses mechanosensitive neurons to detect bacteria, which are food for worms. These neurons release dopamine to suppress foraging and promote dwelling. Through a screen of genes highly expressed in dopaminergic food-sensing neurons, we identify a K2P-family potassium channel-TWK-2-that damps their activity. Strikingly, loss of TWK-2 restores mechanosensation to neurons lacking the NOMPC-like channel transient receptor potential 4 (TRP-4), which was thought to be the primary mechanoreceptor for tactile food sensing. The alternate mechanoreceptor mechanism uncovered by TWK-2 mutation requires three Deg/ENaC channel subunits: ASIC-1, DEL-3, and UNC-8. Analysis of cell-physiological responses to mechanostimuli indicates that TRP and Deg/ENaC channels work together to set the range of analog encoding of stimulus intensity and to improve signal-to-noise characteristics and temporal fidelity of food-sensing neurons. We conclude that a specialized mechanosensory modality-tactile food sensing-emerges from coordination of distinct force-sensing mechanisms housed in one type of sensory neuron.