期刊
ISCIENCE
卷 25, 期 1, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.isci.2021.103562
关键词
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资金
- Canada Graduate Scholarship from NSERC
- Toronto COVID-19 Action Fund
- Canadian Institutes of Health Research Foundation [FDN-154338]
The imbalance in immune response observed in SARS-CoV-2 infected patients may be due to the altered interaction between the nucleocapsid protein (N protein) and stress granule resident proteins, which in turn affects the stress response of host cells.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) nucleocapsid (N) protein is essential for viral replication, making it a promising target for antiviral drug and vaccine development. SARS-CoV-2 infected patients exhibit an uncoordinated immune response; however, the underlying mechanistic details of this imbalance remain obscure. Here, starting from a functional proteomics workflow, we cataloged the protein-protein interactions of SARS-CoV-2 proteins, including an evolutionarily conserved specific interaction of N with the stress granule resident proteins G3BP1 and G3BP2. N localizes to stress granules and sequesters G3BPs away from their typical interaction partners, thus attenuating stress granule formation. We found that N binds directly to host mRNAs in cells, with a preference for 3' UTRs, and modulates target mRNA stability. We show that the N protein rewires the G3BP1 mRNA-binding profile and suppresses the physiological stress response of host cells, which may explain the imbalanced immune response observed in SARS-CoV-2 infected patients.
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