Mechanical strain stimulates COPII-dependent secretory trafficking via Rac1

ABSTRACT: Cells are constantly exposed to various chemical and physical stimuli. While much has been learned about the biochemical factors that regulate secretory trafficking from the endoplasmic reticulum (ER), much less is known about whether and how this trafficking is subject to regulation by mechanical signals. Here we show that subjecting cells to mechanical strain both induces the formation of ER exit sites (ERES) and accelerates ER-to-Golgi trafficking. We found that cells with impaired ERES function were less capable of expanding their surface area when placed under mechanical stress and were more prone to develop plasma membrane defects when subjected to stretching. Thus, coupling of ERES function to mechanotransduction appears to confer resistance of cells to mechanical stress. Furthermor

SUBMITTER: Dr. Santosh Phuyal 

PROVIDER: S-SCDT-EMBOJ-2022-110596 | biostudies-other |

REPOSITORIES: biostudies-other