Touch sensation requires the mechanically gated ion channel ELKIN1

• 成果类型: Article
• 署名作者: Chakrabarti, Sampurna; Klich, Jasmin D.; Khallaf, Mohammed A.; Hulme, Amy J.; Sanchez-Carranza, Oscar; Baran, Zuzanna M.; Rossi, Alice; Huang, Angela Tzu-Lun; Pohl, Tobias; Fleischer, Raluca; Fuerst, Carina; Hammes, Annette; Begay, Valerie; Hoernberg, Hanna; Finol-Urdaneta, Rocio K.; Poole, Kate; Dottori, Mirella; Lewin, Gary R.
• 署名单位: Helmholtz Association; Max Delbruck Center for Molecular Medicine; Egyptian Knowledge Bank (EKB); Assiut University; University of Wollongong; Helmholtz Association; Max Delbruck Center for Molecular Medicine; Helmholtz Association; Max Delbruck Center for Molecular Medicine; Humboldt University of Berlin; University of New South Wales Sydney; Free University of Berlin; Humboldt University of Berlin; Charite Universitatsmedizin Berlin
• 刊物名称: SCIENCE
• ISSN/ISSBN: 0036-13671
• DOI: 10.1126/science.adl0495
• 发表日期: 2024-03-01
• 页码: 992-998
• 关键词: protein; piezo2; mechanotransduction; mechanosensation

摘要

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.