Influenza virus infection induces widespread alterations of host cell splicing
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA646750 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12243954_1.fastq.gz | Fastqsanger.gz | |||
| SRR12243954_2.fastq.gz | Fastqsanger.gz | |||
| SRR12243955_1.fastq.gz | Fastqsanger.gz | |||
| SRR12243955_2.fastq.gz | Fastqsanger.gz | |||
| SRR12243956_1.fastq.gz | Fastqsanger.gz |
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Project description:Influenza A viruses (IAV) use diverse mechanisms to interfere with cellular gene expression and thus limit the antiviral responses and/or promote viral replication. Although many RNAseq studies have documented IAV-induced changes in host mRNA abundance, few were designed to allow an accurate quantification of changes in host mRNA splicing. Here we show that IAV infection of human lung cells induces widespread alterations of cellular splicing, with an overall increase in exon inclusion and decrease in intron retention. Over half of the mRNAs that show differential splicing undergo no significant changes in abundance or in their 3’ end termination site, suggesting that IAV can directly manipulate cellular splicing independently of other transcriptional changes. Cross-analysis of the alternative splicing profiles of IAV-infected and RED-depleted cells demonstrates a partial phenocopying of the RED-knock down phenotype in infected cells, suggesting that hijacking of the RED factor by IAVs to promote splicing of their own mRNAs could account for a minor subset of splicing changes in infected cells. All our results can be expored through a Shiny user friendly interface (http://virhostnet.prabi.fr:3838/shinyapps/flu-splicing).
2020-08-31 | GSE154596 | GEO
Project description:Influenza A viruses (IAVs) use diverse mechanisms to interfere with cellular gene expression. Although many RNA-seq studies have documented IAV-induced changes in host mRNA abundance, few were designed to allow an accurate quantification of changes in host mRNA splicing. Here, we show that IAV infection of human lung cells induces widespread alterations of cellular splicing, with an overall increase in exon inclusion and decrease in intron retention. Over half of the mRNAs that show differential splicing undergo no significant changes in abundance or in their 3' end termination site, suggesting that IAVs can specifically manipulate cellular splicing. Among a randomly selected subset of 21 IAV-sensitive alternative splicing events, most are specific to IAV infection as they are not observed upon infection with VSV, induction of interferon expression or induction of an osmotic stress. Finally, the analysis of splicing changes in RED-depleted cells reveals a limited but significant overlap with the splicing changes in IAV-infected cells. This observation suggests that hijacking of RED by IAVs to promote splicing of the abundant viral NS1 mRNAs could partially divert RED from its target mRNAs. All our RNA-seq datasets and analyses are made accessible for browsing through a user-friendly Shiny interface (http://virhostnet.prabi.fr:3838/shinyapps/flu-splicing or https://github.com/cbenoitp/flu-splicing).
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Project description:Competition and interplay between host and viral gene expression programs is a critical determinant of infection susceptibility and a potential target for anti-viral therapies. Viral infection is well documented to induce the expression of numerous host genes that are part of the innate immune response. Here we show that infection of human lung epithelial cells with Influenza A virus (IAV) also induces a broad program of alternative splicing of host genes. While these splicing-regulated genes are not enriched for known regulators of viral infection, we find that many of these genes do modulate the infection and/or replication of IAV in an siRNA screen. Moreover, inhibition of the IAV-induced splicing pattern in several genes tested also reduces viral infection. We further show that approximately a quarter of the IAV-induced splicing events are regulated by hnRNP K, a host protein we have previously implicated in the nuclear speckle-dependent splicing of the IAV M transcript. Notably, hnRNP K abundance at nuclear speckles is increased upon IAV infection. We propose that this change in subnuclear localization may alter the accessibility of hnRNP K for host transcripts, thereby leading to a program of host splicing changes that promote IAV replication.
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