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Mechanism and consequences of herpes simplex virus 1-mediated regulation of host mRNA alternative polyadenylation

ABSTRACT: Mechanism and consequences of herpes simplex virus 1-mediated regulation of host mRNA alternative polyadenylation

PROVIDER: PRJNA634747 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11837371.fastq.gz	Fastqsanger.gz
	SRR11837372.fastq.gz	Fastqsanger.gz
	SRR11837373.fastq.gz	Fastqsanger.gz
	SRR11837374.fastq.gz	Fastqsanger.gz
	SRR11837375.fastq.gz	Fastqsanger.gz

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Mechanism and consequences of herpes simplex virus 1-mediated regulation of host mRNA alternative polyadenylation

Project description:Herpes Simplex virus-1 (HSV-1) causes widespread disruption of transcription termination (DoTT) of RNA polymerase II (RNAPII) mainly by immediate early gene ICP27. Mechanistically, ICP27 directly binds to the essential mRNA 3’ processingfactor CPSF, induces the assembly of a dead-end 3’ processing complex, and blocks mRNA cleavage. Remarkably, ICP27 also acts as a sequence-dependent activator of mRNA 3’ processing for HSV-1 and a subset of host genes. Our results here show that the bimodal activities of ICP27 play a key role in HSV-1-induced alternative polyadenyalation.

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Mechanism and consequences of herpes simplex virus 1-mediated regulation of host mRNA alternative polyadenylation.

Project description:Eukaryotic gene expression is extensively regulated by cellular stress and pathogen infections. We have previously shown that herpes simplex virus 1 (HSV-1) and several cellular stresses cause widespread disruption of transcription termination (DoTT) of RNA polymerase II (RNAPII) in host genes and that the viral immediate early factor ICP27 plays an important role in HSV-1-induced DoTT. Here, we show that HSV-1 infection also leads to widespread changes in alternative polyadenylation (APA) of host mRNAs. In the majority of cases, polyadenylation shifts to upstream poly(A) sites (PAS), including many intronic PAS. Mechanistically, ICP27 contributes to HSV-1-mediated APA regulation. HSV-1- and ICP27-induced activation of intronic PAS is sequence-dependent and does not involve general inhibition of U1 snRNP. HSV1-induced intronic polyadenylation is accompanied by early termination of RNAPII. HSV-1-induced mRNAs polyadenylated at intronic PAS (IPA) are exported into the cytoplasm while APA isoforms with extended 3' UTRs are sequestered in the nuclei, both preventing the expression of the full-length gene products. Finally we provide evidence that HSV-induced IPA isoforms are translated. Together with other recent studies, our results suggest that viral infection and cellular stresses induce a multi-faceted host response that includes DoTT and changes in APA profiles.

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