Abstract The slightest touch to the skin initiates tactile perception that is almost immediate 1 . The extraordinary speed of touch perception is enabled by mechanically-activated ion channels, the opening of which excites the endings of sensory neurons innervating the skin to initiate sensation. Here we identify a new mechanically-activated ion channel, Elkin1 2 , that, when ablated in mice, leads to a profound behavioural touch insensitivity. Touch insensitivity in Elkin1 -/- mice was caused by a loss of mechanically-activated currents (MA-currents) in around half of all sensory neurons that are activated by light touch (low threshold mechanoreceptors, LTMRs). Reintroduction of Elkin1 into sensory neurons from Elkin1 -/- mice acutely restored MA-currents. Piezo2 3–6 is an established mechanosensitive ion channel required for touch sensation. In mice genetic ablation of Piezo2 renders many, but not all, LTMRs insensitive to mechanical force 4,5,7 . Here we show that Elkin1 underpins PIEZO2-independent touch sensation. Additionally, we find that Elkin1 is present in many nociceptive sensory neurons which detect potentially damaging and painful mechanical force. These nociceptors depend on Elkin1 for effectively communicating information on sustained noxious mechanical forces. We further identified molecular and functional interactions between the known mechanotransduction protein Stoml3 8,9 and Elkin1 ion channels. Our data identify Elkin1 as a novel core component of touch transduction in mammals. The specific sensory deficits exhibited by Elkin1 -/- mice make Elkin1 a highly desirable target that could be harnessed to treat somatic sensory disorders including pain.

Touch sensation requires the mechanically-gated ion channel Elkin1