Abstract
The Target of Rapamycin Complex 2 (TORC2) plays a key role in maintaining the homeostasis of plasma membrane (PM) tension. TORC2 activation upon increased PM tension involves redistribution of the Slm1 and 2 paralogs from PM invaginations known as eisosomes into membrane compartments containing TORC2. How Slm1/2 relocalization is triggered, and if/how this plays a role in TORC2 inactivation upon decreased PM tension is unknown. Using osmotic shocks and Palmitoylcarnitine (PalmC) as orthogonal tools to manipulate PM tension, we demonstrate that decreased PM tension triggers spontaneous, energy-independent reorganization of pre-existing phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) into discrete invaginated membrane domains which cluster and inactivate TORC2. These results demonstrate that an increase and a decrease in membrane tension are sensed through different mechanisms and highlight a role for membrane lipid phase separation in mechanotransduction.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
