Interaction between host G3BP and viral nucleocapsid protein regulates SARS-CoV-2 replication.
Ontology highlight
ABSTRACT: G3BP1/2 are paralogous proteins that promote stress granule formation in response to cellular stresses, including viral infection. G3BP1/2 are prominent interactors of the nucleocapsid (N) protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, the functional consequences of the G3BP1-N interaction in the context of viral infection remain unclear. Here we used structural and biochemical analyses to define the residues required for G3BP1-N interaction, followed by structure-guided mutagenesis of G3BP1 and N to selectively and reciprocally disrupt their interaction. We found that mutation of F17 within the N protein led to selective loss of interaction with G3BP1 and consequent failure of the N protein to disrupt stress granule assembly. Introduction of SARS-CoV-2 b
SUBMITTER: Yang Z
PROVIDER: S-EPMC10327126 | biostudies-literature | 2023 Jun
REPOSITORIES: biostudies-literature
ACCESS DATA