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BET proteins bind the lytic origins of replication [MutuI ChIP-seq]

ABSTRACT: BET proteins bind the lytic origins of replication [MutuI ChIP-seq]

OTHER RELATED OMICS DATASETS IN: GSE84209GSE84212GSE84213GSE84210GSE84214GSE84211GSE98772GSE98773

PROVIDER: PRJNA328409 | ENA |

REPOSITORIES: ENA

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BET proteins bind the lytic origins of replication [MutuI ChIP-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The ChIP-seq data below show that the BET proteins bind to both EBV lytic origins of replication.

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JQ1 prevents BRD4 recruitment to the lytic origins of replication [Akata-Zta Brd4 ChIP-seq]

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BET inhibitors suppress lytic DNA replication [Akata-Zta DNA-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The sequenced total DNA data below show that JQ1 and I-BET cause a decrease in EBV genome replication after induction.

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Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The RNA-seq data below show that the second block causes a decrease in expression of late but not early lytic genes.

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Project description:BET inhibitors suppress lytic DNA replication [Akata-Zta DNA-seq]

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Project description:BET inhibitors suppress lytic DNA replication [Akata-Zta RNA-seq]

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New non-coding lytic transcripts derived from the Epstein Barr virus latency origin of replication oriP are hyper-edited, bind the paraspeckle protein, NONO/p54nrb, and support lytic viral transcription

Project description:We have previously shown that the Epstein-Barr virus (EBV) likely encodes hundreds of viral long non-coding RNAs (vlncRNAs) that are expressed during reactivation. Here we show that the EBV latency origin of replication (oriP) is transcribed bi-directionally during reactivation and that both leftward (oriPtLs) and rightward transcripts (oriPtRs) are largely localized in the nucleus. While the oriPtLs are most likely non-coding, at least some of the oriPtRs contain the BCRF1/vIL10 open reading frame. Nonetheless, oriPtR transcripts with long 5’UTRs may partially serve non-coding functions. Both oriPtL and oriPtR transcripts are expressed with late kinetics and their expression is inhibited by phosphonoacetic acid. RNA-seq analysis showed that oriPtLs and oriPtRs exhibited extensive “hyper-editing” at their Family of Repeat (FR) regions. RNA secondary structure prediction revealed that the FR region of both oriPtLs and oriPtRs may form large evolutionarily conserved and thermodynamically stable hairpins. The double-stranded RNA-binding protein and RNA-editing enzyme ADAR was found to bind to oriPtLs, likely facilitating editing of the FR hairpin. Further, the multifunctional paraspeckle protein, NONO, was found to bind to oriPt transcripts suggesting that oriPts interacts with the paraspeckle-based innate anti-viral immune pathway. Knock-down and ectopic expression of oriPtLs showed that it contributes to global viral lytic gene expression and viral DNA replication. Together, these results show that these new vlncRNAs interact with cellular innate immune pathways and that they help facilitate progression of the viral lytic cascade. RNA-seq analysis for oriPtL knockdown and overexpression experiments

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Project description:JQ1 prevents BRD4 recruitment to the lytic origins of replication [Akata-Zta DNA-seq]

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