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Efficient mRNA processing prevents gene gating-associated replication stress in mammalian cells

ABSTRACT: Efficient mRNA processing prevents gene gating-associated replication stress in mammalian cells

PROVIDER: PRJNA486813 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7723180.fastq.gz	Fastqsanger.gz
	SRR7723181.fastq.gz	Fastqsanger.gz
	SRR7723182.fastq.gz	Fastqsanger.gz
	SRR7723183.fastq.gz	Fastqsanger.gz
	SRR7723184.fastq.gz	Fastqsanger.gz

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Efficient mRNA processing prevents gene gating-associated replication stress in mammalian cells

Project description:Cellular mechanisms that safeguard genome integrity are often subverted in cancer. To identify novel cancer-related genome caretakers, we employed a convergent multi-screening strategy coupled to quantitative image-based cytometry, and ranked candidate genes according to multivariate read-outs reflecting viability, proliferative capacity, replisome integrity and DNA damage signaling. This revealed new regulators of replication stress resilience, including components of the pre-mRNA cleavage and polyadenylation complex. We show that deregulation of pre-mRNA cleavage impairs replication fork speed and leads to excessive origin activity, rendering cells highly dependent on ATR kinase activity. Surprisingly, while excessive formation of RNA:DNA-hybrids under these conditions appears mainly as consequence rather than cause of DNA damage, inhibition of transcription rescued fork speed, origin activation and alleviated replication catastrophe. Importantly, uncoupling pre-mRNA processing from nuclear export by depleting the THO complex also protected cells from DNA damage, suggesting that efficient pre-mRNA cleavage provides a mechanism to prevent gene gating-associated genomic instability.

2019-01-10 | GSE118795 | GEO

CBX3 Regulates Efficient RNA Processing Genome Wide

Project description:HP1 alpha, beta, and gamma play an evolutionarily conserved role in the formation and maintenance of heterochromatin. In addition, some HP1 family members may also participate in transcriptional regulation of genes. Recently, HP1 gamma binding to the bodies of a subset of genes has been observed in human and murine cells. However, the generality of this phenomenon and the role HP1 gamma may play in this context are unknown. Genome-wide localization analysis reveals broad and general HP1 gamma binding at actively transcribed genes, which strongly correlates with gene activity across multiple cell types. Unexpectedly, we find HP1 gamma binding is necessary for efficient RNA processing of its target genes. Loss of HP1 gamma results in defective recruitment of splicing factors including U1-70K, and leads to accumulation of unspliced nascent transcripts genome-wide. Therefore, our data argue that the primary role of HP1 gamma is to ensure efficient RNA processing in mammalian cells. Genome-wide localization and function of HP1 gamma in multiple cell types using ChIP-chip, ChIP-seq, and RNA-seq

2012-05-24 | E-GEOD-28115 | biostudies-arrayexpress

CBX3 Regulates Efficient RNA Processing Genome Wide

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Efficient in vivo genome editing prevents hypertrophic cardiomyopathy in mice

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Adenovirus prevents dsRNA formation by promoting efficient splicing of viral RNA

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Efficient in vivo Genome Editing Prevents Hypertrophic Cardiomyopathy in Mice [Nuc-Seq]

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Adenovirus prevents dsRNA formation by promoting efficient splicing of viral RNA

Project description:Eukaryotic cells recognize intracellular pathogens through pattern recognition receptors, including sensors of aberrant nucleic acid structures. Sensors of double-stranded RNA (dsRNA) are known to detect replication intermediates of RNA viruses. It has been suggested that annealing of mRNA from symmetrical transcription of both top and bottom strands of DNA virus genomes can produce dsRNA during infection. Supporting this hypothesis, nearly all DNA viruses encode inhibitors of dsRNA-recognition pathways. However, direct evidence that DNA viruses produce dsRNA is lacking. Contrary to dogma, we show that the nuclear-replicating DNA virus adenovirus (AdV) does not produce detectable levels of dsRNA during infection. In contrast, abundant dsRNA is detected within the nucleus of cells infected with AdV mutants that lack the virus-directed ubiquitin ligase required for efficient processing of viral RNA. In the presence of nuclear dsRNA, the cytoplasmic dsRNA sensor PKR is relocalized and activated within the nucleus. Accumulation of viral dsRNA occurs in the late phase of infection, when unspliced viral transcripts form intron/exon base pairs between top and bottom strand transcripts. We propose that DNA viruses actively promote efficient splicing and mRNA processing to limit dsRNA formation, thus avoiding detection and restriction by host nucleic acid sensors.

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