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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE149376 | GEO | 2020/05/01

REPOSITORIES: GEO

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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 [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]

2020-05-01 | GSE149374 | GEO

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

2020-05-01 | GSE149373 | GEO

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

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 [MiDA-seq]

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

| PRJNA628521 | ENA

Genome-wide high-resolution mapping of chromosome fragile sites in Saccharomyces cerevisiae.

Project description:In mammalian cells, perturbations in DNA replication result in chromosome breaks in regions termed "fragile sites." Using DNA microarrays, we mapped recombination events and chromosome rearrangements induced by reduced levels of the replicative DNA polymerase-? in the yeast Saccharomyces cerevisiae. We found that the recombination events were nonrandomly associated with a number of structural/sequence motifs that correlate with paused DNA replication forks, including replication-termination sites (TER sites) and binding sites for the helicase Rrm3p. The pattern of gene-conversion events associated with cross-overs suggests that most of the DNA lesions that initiate recombination between homologs are double-stranded DNA breaks induced during S or G2 of the cell cycle, in contrast to spontaneous recombination events that are initiated by double-stranded DNA breaks formed prior to replication. Low levels of DNA polymerase-? also induced very high rates of aneuploidy, as well as chromosome deletions and duplications. Most of the deletions and duplications had Ty retrotransposons at their breakpoints.

| S-EPMC4040566 | biostudies-literature

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