Journal
JOURNAL OF VIROLOGY
Volume 84, Issue 24, Pages 12619-12627Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01696-10
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Funding
- Ministry of Science and Technology of China [2007DFC30240, 2004BA519A64, 2009ZX10004-101, 2008ZX10002-009]
- Chinese Academy of Sciences [KSCX2-YW-R-198, KSCX2-YW-N-054]
- Innovative Research Group of the National Natural Science Foundation of China (NSFC) [81021003]
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Influenza virus RNA-dependent RNA polymerase scavenges the 5' cap from host pre-mRNA to prime viral transcription initiation. It is also well established that viral RNA-dependent RNA polymerase (vRNP) associates with cellular RNA polymerase II (Pol II), on which viral replication depends. Here we report that cyclin T1/CDK9 can interact with influenza virus polymerase and facilitate its association with cellular Pol II. The immunodepletion of cyclin T1/CDK9 totally abolished the association of vRNP with the C-terminal domain (CTD) Ser-2-phosphorylated form of RNA polymerase II. Further studies showed that overexpression of cyclin T1/CDK9 increased the transcription activity of vRNP, while knockdown of cyclin T1/CDK9 impaired viral replication. Our results suggest that cyclin T1/CDK9 serves as an adapter to mediate the interaction of vRNP and RNA Pol II and promote viral transcription.
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