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Cell Microbiol. 2019 May 3:e13038. doi: 10.1111/cmi.13038. [Epub ahead of print]
Influenza virus matrix protein M1 interacts with SLD5 to block host cell cycle.
Zhu L1,2, Zhao W1, Lu J1, Li S1,2, Zhou K1, Jiang W1, Duan X1, Fu L1, Yu B3, Cai KQ4, Gao GF1, Liu W1, Fang M1,3,5.
Author information
Abstract
Influenza virus matrix 1 protein (M1) is highly conserved and plays essential roles at many stages of virus life cycle. Here we used a yeast two-hybrid system to identify the host protein SLD5, a component of the GINS complex, which is essential for the initiation of DNA replication in eukaryotic cells, as a new M1 interacting protein. M1 from several different influenza virus strains all interacted with SLD5. Overexpression of SLD5 suppressed influenza virus replication. Transient, stable or inducible expression of M1 induced host cell cycle blockade at G0/G1 phase. Moreover, SLD5 partially rescued M1 expression- or influenza virus infection- induced G0/G1 phase accumulation in cell lines and primary mouse embryonic fibroblasts. Importantly, SLD5 transgenic mice exhibited higher resistance and improved lung epithelial regeneration after virus infection compared to wild type mice. Therefore, influenza virus M1 blocks host cell cycle process by interacting with SLD5. Our finding reveals the multifunctional nature of M1 and provides new insight for understanding influenza virus-host interaction.
This article is protected by copyright. All rights reserved.
KEYWORDS:
Cell cycle; Influenza virus; Lung epithelial regeneration; M1 protein; SLD5
PMID: 31050118 DOI: 10.1111/cmi.13038
Influenza virus matrix protein M1 interacts with SLD5 to block host cell cycle.
Zhu L1,2, Zhao W1, Lu J1, Li S1,2, Zhou K1, Jiang W1, Duan X1, Fu L1, Yu B3, Cai KQ4, Gao GF1, Liu W1, Fang M1,3,5.
Author information
Abstract
Influenza virus matrix 1 protein (M1) is highly conserved and plays essential roles at many stages of virus life cycle. Here we used a yeast two-hybrid system to identify the host protein SLD5, a component of the GINS complex, which is essential for the initiation of DNA replication in eukaryotic cells, as a new M1 interacting protein. M1 from several different influenza virus strains all interacted with SLD5. Overexpression of SLD5 suppressed influenza virus replication. Transient, stable or inducible expression of M1 induced host cell cycle blockade at G0/G1 phase. Moreover, SLD5 partially rescued M1 expression- or influenza virus infection- induced G0/G1 phase accumulation in cell lines and primary mouse embryonic fibroblasts. Importantly, SLD5 transgenic mice exhibited higher resistance and improved lung epithelial regeneration after virus infection compared to wild type mice. Therefore, influenza virus M1 blocks host cell cycle process by interacting with SLD5. Our finding reveals the multifunctional nature of M1 and provides new insight for understanding influenza virus-host interaction.
This article is protected by copyright. All rights reserved.
KEYWORDS:
Cell cycle; Influenza virus; Lung epithelial regeneration; M1 protein; SLD5
PMID: 31050118 DOI: 10.1111/cmi.13038