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G2/M DNA synthesis at transcription start sites because of RNA transcription persistence during DNA replication [Chip-Seq H2AX]

ABSTRACT: G2/M DNA synthesis at transcription start sites because of RNA transcription persistence during DNA replication [Chip-Seq H2AX]

PROVIDER: PRJNA674611 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12980228_1.fastq.gz	Fastqsanger.gz
	SRR12980228_2.fastq.gz	Fastqsanger.gz
	SRR12980229_1.fastq.gz	Fastqsanger.gz
	SRR12980229_2.fastq.gz	Fastqsanger.gz
	SRR12980230_1.fastq.gz	Fastqsanger.gz

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G2/M DNA synthesis at transcription start sites because of RNA transcription persistence during DNA replication [Chip-Seq H2AX]

Project description:RNA transcription and DNA replication both use DNA as a substrate, that however can be engaged only by one of them at any given time. Consequently, conflicts between transcription and replication significantly affect genome stability and human health. To understand the reciprocal interplay between transcription and replication in human cells, we performed a genome-wide analysis of the two processes throughout S-phase. We found that transcription persists during replication, with direct consequences for replication progression through genes and sites of DNA damage. Importantly however, we also found that transcription start sites will not be replicated together with the surrounding regions, and remain under-replicated throughout S-phase. DNA synthesis across transcription start sites occurs specifically when cells enter mitosis, because the RNA Polymerase II is removed at that point from the majority of the genes. Intriguingly, this G2/M DNA synthesis is not associated with increased DNA damage and occurs at very high frequency.

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G2/M DNA synthesis at transcription start sites because of RNA transcription persistence during DNA replication

Project description:G2/M DNA synthesis at transcription start sites because of RNA transcription persistence during DNA replication

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High mobility group protein-mediated transcription requires DNA damage marker γ-H2AX

Project description:The eukaryotic genome is organized into chromatins, the physiological template for DNA-dependent processes including replication, recombination, repair, and transcription. Chromatin-mediated transcription regulation involves DNA methylation, chromatin remodeling, and histone modifications. However, chromatin also contains non-histone chromatin-associated proteins, of which the high-mobility group (HMG) proteins are the most abundant. Although it is known that HMG proteins induce structural changes of chromatin, the processes underlying transcription regulation by HMG proteins are poorly understood. Here we decipher the molecular mechanism of transcription regulation mediated by the HMG AT-hook 2 protein (HMGA2). We combined proteomic, ChIP-seq, and transcriptome data to show that HMGA2-induced transcription requires phosphorylation of the histone variant H2AX at S139 (H2AXS139ph; γ-H2AX) mediated by the protein kinase ataxia telangiectasia mutated (ATM). Furthermore, we demonstrate the biological relevance of this mechanism within the context of TGFβ1 signaling. The interplay between HMGA2, ATM, and H2AX is a novel mechanism of transcription initiation. Our results link H2AXS139ph to transcription, assigning a new function for this DNA damage marker. Controlled chromatin opening during transcription may involve intermediates with DNA breaks that may require mechanisms that ensure the integrity of the genome.

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