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Genome-wide analysis of DNA replication by TrAEL-seq in mouse embryonic stem cells

ABSTRACT: Genome-wide analysis of DNA replication by TrAEL-seq in mouse embryonic stem cells

PROVIDER: PRJNA1081367 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28121935.fastq.gz	Fastqsanger.gz
	SRR28121936.fastq.gz	Fastqsanger.gz
	SRR28121937.fastq.gz	Fastqsanger.gz
	SRR28121938.fastq.gz	Fastqsanger.gz

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Genome-wide analysis of DNA replication by TrAEL-seq in mouse embryonic stem cells

Project description:We have applied the TrAEL-seq method to profile DNA replication in wild type and Snf2h knockoutmouse embryonic stem cells.

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Genome-wide analysis of DNA replication and double strand breaks by TrAEL-seq

Project description:We have designed a methodology for capture of DNA 3’ ends that allows mapping of resected DNA breaks, stalled replication forks and also normal replication fork progression. This Transferase-activated end ligation or TrAEL-seq method involves ligation of a functionalised linker to DNA 3’ ends followed by fragmentation, purification of adaptor ligated fragments, second adaptor ligation and library amplification. The major advantages of TrAEL-seq compared to other available methods are: i) an ability to map double strand breaks after resection, ii) excellent sensitivity and signal-to-noise in detecting replication fork stalling and iii) ability to map replication fork progression in unsynchronised, unlabelled populations of both yeast and mammalian cells. The samples provided here were selected to demonstrate different aspects of TrAEL-seq activity: the SfiI and dmc1 datasets shows capture of 3’ extended single strand DNA. The other yeast datasets show replication and replication fork stalling information. The RAF and RAF-GAL grown yeast samples show the effect transcriptional induction on replication fork progression. The hESC samples show the capacity to derive replication profiles from mammalian cells.

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Genome-wide analysis of DNA replication and double strand breaks by TrAEL-seq

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Genome-wide analysis of DNA replication stress in the Human Neuroblastoma Cell Line IMR32 by TrAEL-seq

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Genome-wide analysis of replication fork locations in hydroxyurea-treated Saccharomyces cerevisiae by TrAEL-seq

Project description:Genome-wide analysis of replication fork locations in hydroxyurea-treated Saccharomyces cerevisiae by TrAEL-seq

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Genome-wide analysis of DNA replication and DNA double-strand breaks using TrAEL-seq.

Project description:Faithful replication of the entire genome requires replication forks to copy large contiguous tracts of DNA, and sites of persistent replication fork stalling present a major threat to genome stability. Understanding the distribution of sites at which replication forks stall, and the ensuing fork processing events, requires genome-wide methods that profile replication fork position and the formation of recombinogenic DNA ends. Here, we describe Transferase-Activated End Ligation sequencing (TrAEL-seq), a method that captures single-stranded DNA 3' ends genome-wide and with base pair resolution. TrAEL-seq labels both DNA breaks and replication forks, providing genome-wide maps of replication fork progression and fork stalling sites in yeast and mammalian cells. Replication maps are similar to those obtained by Okazaki fragment sequencing; however, TrAEL-seq is performed on asynchronous populations of wild-type cells without incorporation of labels, cell sorting, or biochemical purification of replication intermediates, rendering TrAEL-seq far simpler and more widely applicable than existing replication fork direction profiling methods. The specificity of TrAEL-seq for DNA 3' ends also allows accurate detection of double-strand break sites after the initiation of DNA end resection, which we demonstrate by genome-wide mapping of meiotic double-strand break hotspots in a dmc1Δ mutant that is competent for end resection but not strand invasion. Overall, TrAEL-seq provides a flexible and robust methodology with high sensitivity and resolution for studying DNA replication and repair, which will be of significant use in determining mechanisms of genome instability.

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Project description:Pluripotent stem cells can give rise to the three embryonic germ layers and the characterization of their properties is crucial to exploit their therapeutic potential. Mouse embryonic stem cells (mESCs) are isolated and usually maintained in vitro in a primed state that resembles the post-implantation epiblast features. Furthermore, primed mESCs can be de-differentiated to a naive state that resembles the pre-implantation inner cell mass (ICM). Cell differentiation or genotoxic stress, among others, can alter DNA replication, which is a flexible process able to adapt to different cellular contexts. Here, we demonstrate that primed-to-naive mESC reprogramming triggers replication fork slowdown, increased fork asymmetry and a compensatory activation of dormant origins. Using iPOND (“isolation of proteins on nascent DNA”) coupled to mass spectrometry we have characterized the changes in replisome composition between naive and primed mESCs. Several DNA repair factors, including MRE11 nuclease, are enriched in naive mESCs forks, while factors involved in ubiquitin-dependent protein metabolism are enriched in primed mESC forks. We report that primed-to-naive mESC de-differentiation promotes recruitment of MRE11 to the forks in response to transcription-replication conflicts, underlying the DNA replication rewiring required for efficient mESC reprogramming.

2024-04-03 | PXD041946 | Pride

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