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CDK9 and SPT5 proteins are specifically required for expression of herpes simplex virus 1 replication-dependent late genes

Journal article
Authors Zhiyuan Zhao
Ka-Wei Tang
Isabella Muylaert
Tore Samuelsson
Per Elias
Published in Journal of Biological Chemistry
Volume 292
Issue 37
Pages 15489-15500
ISSN 0021-9258
Publication year 2017
Published at Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 15489-15500
Language en
Links doi.org/10.1074/jbc.M117.806000
Keywords rna-polymerase-ii, thymidine kinase gene, type-1 late gene, transcription elongation, p-tefb, terminal domain, tata box, macromolecular-synthesis, infected-cells, messenger-rna, Biochemistry & Molecular Biology, knight sl, 1981, cell, v25, p385, knight sl, 1984, cell, v37, p253
Subject categories Biological Sciences

Abstract

DNA replication greatly enhances expression of the herpes simplex virus 1 (HSV-1) gamma 2 late genes by still unknown mechanisms. Here, we demonstrate that 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), an inhibitor of CDK9, suppresses expression of gamma 2 late genes with an IC50 of 5 mu M, which is at least 10 times lower than the IC50 value required for inhibition of expression of early genes. The effect of DRB could not be explained by inhibition of DNA replication per se or loading of RNA polymerase II to late promoters and subsequent reduction of transcription. Instead, DRB reduces accumulation of gamma 2 late mRNA in the cytoplasm. In addition, we show that siRNA-mediated knockdown of the transcription factor SPT5, but not NELF-E, also gives rise to a specific inhibition of HSV-1 late gene expression. Finally, addition of DRB reduces co-immunoprecipitation of ICP27 using an anti-SPT5 antibody. Our results suggest that efficient expression of replication-dependent gamma 2 late genes is, at least in part, regulated by CDK9 dependent co-and/or post-transcriptional events involving SPT5 and ICP27.

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