
ABSTRACT 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.
Transcription, Genetic, Reverse Transcriptase Polymerase Chain Reaction, Cyclin T, Blotting, Western, Fluorescent Antibody Technique, Kidney, RNA-Dependent RNA Polymerase, Cyclin-Dependent Kinase 9, Dogs, Orthomyxoviridae Infections, Influenza A virus, Influenza, Human, RNA Precursors, Animals, Humans, Immunoprecipitation, RNA Polymerase II, RNA, Messenger, RNA, Small Interfering, Cells, Cultured
Transcription, Genetic, Reverse Transcriptase Polymerase Chain Reaction, Cyclin T, Blotting, Western, Fluorescent Antibody Technique, Kidney, RNA-Dependent RNA Polymerase, Cyclin-Dependent Kinase 9, Dogs, Orthomyxoviridae Infections, Influenza A virus, Influenza, Human, RNA Precursors, Animals, Humans, Immunoprecipitation, RNA Polymerase II, RNA, Messenger, RNA, Small Interfering, Cells, Cultured
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