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Genome-wide High Resolution Mapping of Mitotic DNA Synthesis Sites and Common Fragile Sites by Direct Sequencing [MiDA-seq]

ABSTRACT: Genome-wide High Resolution Mapping of Mitotic DNA Synthesis Sites and Common Fragile Sites by Direct Sequencing [MiDA-seq]

PROVIDER: PRJNA628521 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11612548_1.fastq.gz	Fastqsanger.gz
	SRR11612548_2.fastq.gz	Fastqsanger.gz
	SRR11612549_1.fastq.gz	Fastqsanger.gz
	SRR11612549_2.fastq.gz	Fastqsanger.gz
	SRR11612550_1.fastq.gz	Fastqsanger.gz

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Genome-wide High Resolution Mapping of Mitotic DNA Synthesis Sites and Common Fragile Sites by Direct Sequencing [WGS]

Project description:Common fragile sites (CFSs) are genomic loci prone to the formation of breaks or gaps on metaphase chromosomes. Here, we seek to map human CFSs with high resolution on a genome-wide scale by sequencing the sites of mitotic DNA synthesis (MiDASeq) that are specific for CFSs. We generated a nucleotide-resolution atlas of MiDAS sites (MDSs) that covered most of know CFSs, and comprehensively analyzed their sequence characteristics and genomic features.

2020-05-01 | GSE149375 | GEO

Genome-wide High Resolution Mapping of Mitotic DNA Synthesis Sites and Common Fragile Sites by Direct Sequencing [RNA-seq]

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Genome-wide High Resolution Mapping of Mitotic DNA Synthesis Sites and Common Fragile Sites by Direct Sequencing [MiDA-seq]

2020-05-01 | GSE149373 | GEO

Genome-wide High Resolution Mapping of Mitotic DNA Synthesis Sites and Common Fragile Sites by Direct Sequencing

Project description:Genome-wide High Resolution Mapping of Mitotic DNA Synthesis Sites and Common Fragile Sites by Direct Sequencing

| PRJNA628516 | ENA

Genome-wide High Resolution Mapping of Mitotic DNA Synthesis Sites and Common Fragile Sites by Direct Sequencing [WGS]

Project description:Genome-wide High Resolution Mapping of Mitotic DNA Synthesis Sites and Common Fragile Sites by Direct Sequencing [WGS]

| PRJNA628519 | ENA

Genome-wide High Resolution Mapping of Mitotic DNA Synthesis Sites and Common Fragile Sites by Direct Sequencing [RNA-seq]

Project description:Genome-wide High Resolution Mapping of Mitotic DNA Synthesis Sites and Common Fragile Sites by Direct Sequencing [RNA-seq]

| PRJNA628520 | ENA

Genome-wide high-resolution mapping of mitotic DNA synthesis sites and common fragile sites by direct sequencing.

Project description:Common fragile sites (CFSs) are genomic loci prone to the formation of breaks or gaps on metaphase chromosomes. They are hotspots for chromosome rearrangements and structural variations, which have been extensively implicated in carcinogenesis, aging, and other pathological processes. Although many CFSs were identified decades ago, a consensus is still lacking for why they are particularly unstable and sensitive to replication perturbations. This is in part due to the lack of high-resolution mapping data for the vast majority of the CFSs, which has hindered mechanistic interrogations. Here, we seek to map human CFSs with high resolution on a genome-wide scale by sequencing the sites of mitotic DNA synthesis (MiDASeq) that are specific for CFSs. We generated a nucleotide-resolution atlas of MiDAS sites (MDSs) that covered most of the known CFSs, and comprehensively analyzed their sequence characteristics and genomic features. Our data on MDSs tallied well with long-standing hypotheses to explain CFS fragility while highlighting the contributions of late replication timing and large transcription units. Notably, the MDSs also encompassed most of the recurrent double-strand break clusters previously identified in mouse neural stem/progenitor cells, thus bridging evolutionarily conserved break points across species. Moreover, MiDAseq provides an important resource that can stimulate future research on CFSs to further unravel the mechanisms and biological relevance underlying these labile genomic regions.

| S-EPMC7785011 | biostudies-literature

Genome-wide High Resolution Mapping of Mitotic DNA Synthesis Sites and Common Fragile Sites by Direct Sequencing

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

2020-05-01 | GSE149376 | GEO

Chromatin immunopreciptiation of human lymphoblastoid cells to identify histone H3K9/14 acetylation regions at common fragile sites

Project description:Map the histone H3K9/14 acetylation regions of in human cells at 7 common fragile sites and their flanking non-fragile sequences as well as a 200kb containing the rare fragile site FRAXA, a 1,075kb non-fragile region on chr22, a hyperacetylated region HALPHA44, and a heterochromatic region HET405. The acetylated regions were mapped in untreated, aphidicolin(APH)-treated, trichostatin(TSA)-treated, and TSA plus APH-treated cells by combining the chromatin-immunoprecipitation with a tiled microarray platform (ChIP-chip).

2009-10-07 | E-TABM-347 | biostudies-arrayexpress

High-resolution mapping of mitotic DNA synthesis regions and common fragile sites in the human genome through direct sequencing.

Project description:DNA replication stress, a feature of human cancers, often leads to instability at specific genomic loci, such as the common fragile sites (CFSs). Cells experiencing DNA replication stress may also exhibit mitotic DNA synthesis (MiDAS). To understand the physiological function of MiDAS and its relationship to CFSs, we mapped, at high resolution, the genomic sites of MiDAS in cells treated with the DNA polymerase inhibitor aphidicolin. Sites of MiDAS were evident as well-defined peaks that were largely conserved between cell lines and encompassed all known CFSs. The MiDAS peaks mapped within large, transcribed, origin-poor genomic regions. In cells that had been treated with aphidicolin, these regions remained unreplicated even in late S phase; MiDAS then served to complete their replication after the cells entered mitosis. Interestingly, leading and lagging strand synthesis were uncoupled in MiDAS, consistent with MiDAS being a form of break-induced replication, a repair mechanism for collapsed DNA replication forks. Our results provide a better understanding of the mechanisms leading to genomic instability at CFSs and in cancer cells.

| S-EPMC7784693 | biostudies-literature

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