ER-shaping atlastin proteins act as central hubs to promote flavivirus replication and virion assembly.

ABSTRACT: Flaviviruses, including dengue virus and Zika virus, extensively remodel the cellular endomembrane network to generate replication organelles that promote viral genome replication and virus production. However, it remains unclear how these membranes and associated cellular proteins act during the virus cycle. Here, we show that atlastins (ATLs), a subset of ER resident proteins involved in neurodegenerative diseases, have dichotomous effects on flaviviruses-with ATL2 depletion leading to replication organelle defects, and ATL3 depletion to changes in virus production pathways. We characterized non-conserved functional domains in ATL paralogues and show that the ATL interactome is profoundly reprogrammed following dengue virus infection. Screen analysis confirmed non-redundant ATL functions

SUBMITTER: Neufeldt CJ 

PROVIDER: S-EPMC6881184 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature