Open AccessMammalian TRP ion channels are insensitive to membrane stretch
Author(s) -
Yu. A. Nikolaev,
Charles D. Cox,
Pietro Ridone,
Paul R. Rohde,
Julio F. Cordero-Morales,
Valeria Vásquez,
Derek R. Laver,
Boris Martinac
Publication year - 2019
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.238360
Subject(s) - transient receptor potential channel , stretch activated ion channel , biology , ion channel , diacylglycerol kinase , mechanotransduction , microbiology and biotechnology , biophysics , motility , cell membrane , mechanosensitive channels , membrane , signal transduction , protein kinase c , biochemistry , receptor
TRP channels of the transient receptor potential ion channel superfamily are involved in a wide variety of mechanosensory processes, including touch sensation, pain, blood pressure regulation, bone loading and detection of cerebrospinal fluid flow. However, in many instances it is unclear whether TRP channels are the primary transducers of mechanical force in these processes. In this study, we tested stretch activation of eleven TRP channels from six mammalian subfamilies. We found that these TRP channels were insensitive to short membrane stretches in cellular systems. Furthermore, we purified TRPC6 and demonstrated its insensitivity to stretch in liposomes, an artificial bilayer system free from cellular components. Additionally, we demonstrated that, when expressed in C. elegans neurons, mouse TRPC6 restores the mechanoresponse of a touch insensitive mutant but requires diacylglycerol for activation. These results strongly suggest that the mammalian members of the TRP ion channel family are insensitive to tension induced by cell membrane stretching and, thus, are more likely to be activated by cytoplasmic tethers or downstream components and to act as amplifiers of cellular mechanosensory signaling cascades.