Foot-and-Mouth Disease Virus 3A Hijacks Sar1 and Sec12 for ER Remodeling in a COPII-Independent Manner.

ABSTRACT: Positive-stranded RNA viruses modify host organelles to form replication organelles (ROs) for their own replication. The enteroviral 3A protein has been demonstrated to be highly associated with the COPI pathway, in which factors operate on the ER-to-Golgi intermediate and the Golgi. However, Sar1, a COPII factor exerting coordinated action at endoplasmic reticulum (ER) exit sites rather than COPI factors, is required for the replication of foot-and-mouth disease virus (FMDV). Therefore, further understanding regarding FMDV 3A could be key to explaining the differences and to understanding FMDV's RO formation. In this study, FMDV 3A was confirmed as a peripheral membrane protein capable of modifying the ER into vesicle-like structures, which were neither COPII vesicles nor autophagosomes.

SUBMITTER: Lee HW 

PROVIDER: S-EPMC9028839 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature