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• W2335961331 abstract "Coronaviruses (CoVs) are enveloped RNA viruses containing a ~30 kb positive-sense single-stranded genomic RNA (gRNA), which encodes non-structural proteins involved in viral replication. In addition to the gRNA, several subgenomic mRNAs (sgmRNAs) are generated during viral replication, which encode mainly the structural proteins. All the viral RNAs, including the gRNA and the sgmRNAs, are co-terminal, through a unique discontinuous transcription mechanism during negative-strand RNA synthesis. This discontinuous process is controlled by a conserved transcription regulating sequence (TRS), which is located after the leader sequence (leader TRS) and in front of each gene (body TRS). It has been suggested that through base pairing between the leader TRS and the complementary body TRS, a template-switching event occurs to generate the discontinuous sgmRNAs. However, the molecular mechanisms controlling the switch from discontinuous to continuous transcription in CoV still remain unknown currently. The most abundant viral sgmRNA encodes the viral nucleocapsid (N) protein, which is categorized as a structural protein to form a helical ribonucleoprotein required for packaging gRNA into the virion. N protein also has non-structural functions in regulating the synthesis of viral gRNA as revealed by reverse genetic studies, but the underlying mechanism is remained unclear. Regarding to the N protein as a highly basic protein with substantial phosphorylation modifications, our study demonstrated that the major phosphorylation sites in both SARS-CoV and JHMV are the Ser residues clustered within the central serine–arginine (SR)-rich motif. We also identified the GSK-3 to be the kinase responsible for this phosphorylation. Treatment with GSK-3 inhibitor can reduce the viral titer and cytopathic effects, suggesting this phosphorylation in N protein is relevant to the viral replication cycle.In the current study, we further discovered a novel function of this GSK-3 mediated N phosphorylation in supporting the transition from discontinuous to continuous transcription of JHMV. Suppression of this specific phosphorylation diminished the synthesis of gRNA and larger sgmRNAs but not the smaller ones. It thus suggested this N phosphorylation might participate in the discontinuous transcription process, with function to ensure the synthesis of full length gRNA and successful production of mature virions. We found the cellular DDX1 is recruited to the phosphorylated N-containing complex and facilitates template readthrough when encountering TRSs for the synthesis of longer viral RNAs. Our results thus demonstrate a unique strategy for the transition from discontinuous to continuous transcription in CoVs via the novel function of the GSK-3 phosphorylated viral N protein." @default.
• W2335961331 created "2016-06-24" @default.
• W2335961331 creator A5028687534 @default.
• W2335961331 date "2014-01-01" @default.
• W2335961331 modified "2023-09-27" @default.
• W2335961331 title "冠狀病毒核殼蛋白磷酸化修飾調控病毒 RNA 轉錄過程之分子機制研究" @default.
• W2335961331 doi "https://doi.org/10.6342/ntu.2014.01104" @default.
• W2335961331 hasPublicationYear "2014" @default.
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