Touch sensation requires the mechanically gated ion channel ELKIN1

Abstract

Touch perception is enabled by mechanically activated ion channels, the opening of which excites cutaneous sensory endings to initiate sensation. In this study, we identify ELKIN1 as an ion channel likely gated by mechanical force, necessary for normal touch sensitivity in mice. Touch insensitivity in Elkin1 −/− mice was caused by a loss of mechanically activated currents (MA currents) in around half of all sensory neurons activated by light touch (low-threshold mechanoreceptors). Reintroduction of Elkin1 into sensory neurons from Elkin1 −/− mice restored MA currents. Additionally, small interfering RNA–mediated knockdown of ELKIN1 from induced human sensory neurons substantially reduced indentation-induced MA currents, supporting a conserved role for ELKIN1 in human touch. Our data identify ELKIN1 as a core component of touch transduction in mice and potentially in humans.

Distinct molecular and functional properties of human induced-proprioceptor and low-threshold mechanoreceptor neurons

“…PIEZO2 is a major channel mediating mechanosensation in iPNs and iLTMRs but its reduced expression did not convey functional differences between the two populations. Our previous studies highlighted the significant role of ELKIN1 in mechanosensation for both rodent and human DRG sensory neurons 56 , and similar to other MA channels, expression of ELKIN1 was comparable between iPNs and iLTMRs. The differential expression of ion channel isoforms, as observed with PIEZO2 in iPNs and iLTMRs, may underpin the functional signatures of each mechanosensory subtype.…”