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RNA decay during gammaherpesvirus infection reduces RNA polymerase II occupancy of host promoters but spares viral promoters

ABSTRACT: RNA decay during gammaherpesvirus infection reduces RNA polymerase II occupancy of host promoters but spares viral promoters

PROVIDER: PRJNA548379 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9275600.fastq.gz	Fastqsanger.gz
	SRR9275610.fastq.gz	Fastqsanger.gz
	SRR9275620.fastq.gz	Fastqsanger.gz
	SRR9275601.fastq.gz	Fastqsanger.gz
	SRR9275611.fastq.gz	Fastqsanger.gz

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Herpesvirus infection reduces Pol II occupancy of host promoters but spares viral promoters

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RNA decay during gammaherpesvirus infection reduces RNA polymerase II occupancy of host promoters but spares viral promoters.

Project description:In mammalian cells, widespread acceleration of cytoplasmic mRNA degradation is linked to impaired RNA polymerase II (Pol II) transcription. This mRNA decay-induced transcriptional repression occurs during infection with gammaherpesviruses including Kaposi's sarcoma-associated herpesvirus (KSHV) and murine gammaherpesvirus 68 (MHV68), which encode an mRNA endonuclease that initiates widespread RNA decay. Here, we show that MHV68-induced mRNA decay leads to a genome-wide reduction of Pol II occupancy at mammalian promoters. This reduced Pol II occupancy is accompanied by down-regulation of multiple Pol II subunits and TFIIB in the nucleus of infected cells, as revealed by mass spectrometry-based global measurements of protein abundance. Viral genes, despite the fact that they require Pol II for transcription, escape transcriptional repression. Protection is not governed by viral promoter sequences; instead, location on the viral genome is both necessary and sufficient to escape the transcriptional repression effects of mRNA decay. We propose a model in which the ability to escape from transcriptional repression is linked to the localization of viral DNA within replication compartments, providing a means for these viruses to counteract decay-induced transcript loss.

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Project description:We perform RNA Polymerase II ChIp sequencing on MHV68 infected MC57G B6 mouse fibroblasts alongside a MHV68 mutant (R443I) that is deficient for RNA decay. We profile the occupancy of Pol II on host and viral genes at 24h post infection.We find that host genes have less Pol II occpancy genome wide, while viral genes remain robustly transcribed irrespective of RNA decay.

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