Format

Send to

Choose Destination
J Cell Sci. 2019 Dec 10;132(23). pii: jcs238360. doi: 10.1242/jcs.238360.

Mammalian TRP ion channels are insensitive to membrane stretch.

Author information

1
Molecular Cardiology and Biophysics Division, Victor Chang Cardiac Research Institute, Sydney 2010, Australia.
2
Human Physiology, School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle 2308, Australia.
3
Department of Physiology, College of Medicine, The University of Tennessee Health Science Center, Memphis 38163, USA.
4
Human Physiology, School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle 2308, Australia b.martinac@victorchang.edu.au derek.laver@newcastle.edu.au.
5
Molecular Cardiology and Biophysics Division, Victor Chang Cardiac Research Institute, Sydney 2010, Australia b.martinac@victorchang.edu.au derek.laver@newcastle.edu.au.
6
St. Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney 2052, Australia.

Abstract

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.

KEYWORDS:

Ion channel reconstitution; Mechanosensitive channels; Mechanotransduction; TRP ion channels; TRPC6

PMID:
31722978
DOI:
10.1242/jcs.238360
Free full text

Conflict of interest statement

Competing interestsThe authors declare no competing or financial interests.

Supplemental Content

Full text links

Icon for HighWire
Loading ...
Support Center