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Chromatin states and genomic organization impact local replication features and timing

ABSTRACT: Chromatin states and genomic organization impact local replication features and timing

PROVIDER: PRJNA733482 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14678300.fastq.gz	Fastqsanger.gz
	SRR14678400.fastq.gz	Fastqsanger.gz
	SRR14678301.fastq.gz	Fastqsanger.gz
	SRR14678401.fastq.gz	Fastqsanger.gz
	SRR14678202.fastq.gz	Fastqsanger.gz

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Chromatin states and genomic organization impact local replication features and timing [ChIP-seq]

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Chromatin states and genomic organization impact local replication features and timing [ChIP-seq]

Project description:Replication timing (RT) control is linked to histone modifications (HMs) and genome architecture. However, HM landscape across cell cycle and its relationship with RT and chromatin modifiers have not been comprehensively assessed. Here we perform detailed replication profiling together with cell cycle profiling of multiple HMs, ATAC-seq, and gene expression. We classify 97% of the genome into four gross chromatin states, including a previously uncharacterized intergenic H3K36me2 state. RT and associated replication features (e.g. initiation zones) quantitatively associate with these chromatin states, HM dynamics, and spatial chromatin structure. Furthermore, overexpression of the histone H3 lysine 9/36 tri-demethylase KDM4A impacts RT across 12% of the genome. RT regulation is strongly linked to KDM4A-associated HMs and enhancer-like elements. Lastly, replication within the intergenic H3K36me2 neighborhoods is sensitive to KDM4A overexpression and is controlled as wide megabase-scale units. In conclusion, these studies establish a critical role for chromatin regulation in directing RT genome-wide.

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Project description:Replication timing (RT) associates with genome architecture, while having a mixed relationship to histone marks. By profiling replication at high-resolution and systematically assessing broad and focused histone marks across cell cycle with and without genetic perturbation, we address the causal relationship between histone marks, their associated states and RT. Our approach identified four chromatin states, including a previously uncharacterized H3K36me2 state, that defined 97% of the mappable genome. RT and local replication patterns (e.g., initiation zones) quantitatively associate with chromatin states, histone mark dynamics, and spatial chromatin structure. Furthermore, overexpression of the histone H3 lysine 9/36 tri-demethylase KDM4A impacts RT genome-wide (11%), which is linked to KDM4A-associated histone marks and clusters of enhancer elements. Lastly, replication within H3K36me2-enriched neighborhoods is sensitive to KDM4A overexpression and is controlled at a megabase-scale. These studies establish a critical role for chromatin regulation in regulating RT and the local RT patterns.

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Chromatin states and genomic organization impact local replication features and timing

Project description:This SuperSeries is composed of the SubSeries listed below.

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Replication timing of siRNA control and siRNA PolQRKO cells

Project description:The human A-family DNA polymerase M-NM-8 (Pol q) is a large, multidomain enzyme whose physiological function is still unclear despite its in vitro translesion synthesis capacity in front of DNA damage and its involvement in some features of DNA repair after external stress. Here we present evidence that Pol q holds a novel role in the absence of external stress as a critical determinant of the replication timing program in human cells. Pol q binds to chromatin at early G1 and is required for proper formation of pre-replicative complexe and replication origin activation. Pol q-depleted cells show modified spatial organization of chromatin-loop structures at replication factories. Genome-wide analysis of replication timing shows delayed replication of a part of early replicating domains and advanced replication of a part of late replicating domains following Pol q depletion. Our results identify Pol q as one of the first critical human factors discovered in the replication timing programme. Two-condition experiment, siRNA control vs. siRNA polQ cells. Biological replicates: 2 control replicates, 2 transfected replicates.

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