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Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer

ABSTRACT: Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer

PROVIDER: PRJNA386042 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5520240.fastq.gz	Fastqsanger.gz
	SRR5520260.fastq.gz	Fastqsanger.gz
	SRR5520270.fastq.gz	Fastqsanger.gz
	SRR5520280.fastq.gz	Fastqsanger.gz
	SRR5520241.fastq.gz	Fastqsanger.gz

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Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer [Bisulfite-Seq]

Project description:DNA replication timing is known to facilitate the establishment of the epigenome, however, the intimate connection between replication timing and changes to the genome and epigenome in cancer remain largely uncharacterised. Here, we perform Repli-Seq and integrated epigenome analyses and demonstrate that genomic regions that undergo long-range epigenetic deregulation in prostate cancer also show concordant differences in replication timing. A subset of altered replication timing domains are conserved across cancers from different tissue origins. Notably, late-replicating regions in cancer cells display a loss of DNA methylation, and a switch in heterochromatin features from H3K9me3-marked constitutive to H3K27me3-marked facultative heterochromatin. Finally, analysis of 214 prostate and 35 breast cancer genomes reveal that late-replicating regions are prone to cis and early-replication to trans chromosomal rearrangements. Together, our data suggests that the nature of chromosomal rearrangement in cancer is related to the spatial and temporal positioning and altered epigenetic states of early-replicating compared to late-replicating loci.

2019-01-23 | GSE124274 | GEO

Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer [Repli-seq]

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Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer [ChIP-seq]

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Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer [Bisulfite-Seq]

Project description:Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer [Bisulfite-Seq]

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Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer.

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Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer

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

2019-01-23 | GSE98732 | GEO

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Project description:Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer [Repli-seq]

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Project description:Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer [ChIP-seq]

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Analysis of Gross Chromosomal Rearrangements in Budding Yeast

Project description:Determine changes in genomic copy across the entire genome for isolated strains with selected gross chromosomal rearrangements relative to the wild-type strain.

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Project description:Chromosomal rearrangements are essential events in the pathogenesis of both malignant and nonmalignant disorders, yet the factors affecting their formation are incompletely understood. We developed a zinc finger nuclease translocation reporter (ZITR) and screened for factors that modulate rearrangements in human cells. We identified UBC9 and RAD50 as suppressors and 53BP1, DDB1, and PARP3 as promoters of chromosomal rearrangements across human cell types. We focused on poly(ADP)ribose polymerase 3 (PARP3) as it is dispensable for murine viability and has druggable catalytic activity. We found that PARP3 regulated G quadruplex (G4) DNA in response to DNA damage, which suppressed repair by nonhomologous end-joining and homologous recombination. Chemical stabilization of G4 DNA in PARP3-/- cells led to widespread DNA double-strand breaks and synthetic lethality. We propose a model in which PARP3 suppresses G4 DNA and facilitates DNA repair by multiple pathways.

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