ER/Golgi trafficking is facilitated by unbranched actin filaments containing Tpm4.2.

ABSTRACT: We have identified novel actin filaments defined by tropomyosin Tpm4.2 at the ER. EM analysis of mouse embryo fibroblasts (MEFs) isolated from mice expressing a mutant Tpm4.2 (Tpm4^Plt53/Plt53 ), incapable of incorporating into actin filaments, revealed swollen ER structures compared with wild-type (WT) MEFs (Tpm4^+/+ ). ER-to-Golgi, but not Golgi-to-ER trafficking was altered in the Tpm4^Plt53/Plt53 MEFs following the transfection of the temperature sensitive ER-associated ts045-VSVg construct. Exogenous Tpm4.2 was able to rescue the ER-to-Golgi trafficking defect in the Tpm4^Plt53/Plt53 cells. The treatment of WT MEFs with the myosin II inhibitor, blebbistatin, blocked the Tpm4.2-dependent ER-to-Golgi trafficking. The lack of an effect on ER-to-Gol

SUBMITTER: Kee AJ 

PROVIDER: S-EPMC7971414 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature