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Replication timing data for six human cell lines under aphidicolin treatment (t0) and after release (N+1)

ABSTRACT: Replication timing data for six human cell lines under aphidicolin treatment (t0) and after release (N+1)

PROVIDER: PRJNA658525 | ENA |

REPOSITORIES: ENA

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Replication timing data for six human cell lines under aphidicolin treatment (t0) and after release (N+1)

Project description:DNA replication is very well orchestrated in mammalian cells due to a tight regulation of the temporal order of replication origin activation, known as the replication timing program. The replication timing of a given replication domain is very robust and well conserved in each cell type. Upon low replication stress, the slowing of replication forks induces delayed replication of some fragile regions leading to DNA damage and genetic instability. Except for these fragile regions, the direct impact of low replication stress on the replication timing in different cellular backgrounds has not been explored in detail. Here we analysed DNA replication timing across the whole genome in a panel of human cell lines in the presence of low replication stress. We demonstrate that low replication stress induced by aphidicolin has a stronger impact on the replication timing of cancer cells than non-tumour cells. Strikingly, we unveiled an enrichment of specific replication domains undergoing a switch from late to early replication in some cancer cells. We found that advances in replication timing correlate with heterochromatin regions poorly sensitive to DNA damage signalling while being subject to an increase of chromatin accessibility in response to aphidicolin. Finally, our data indicate that, following release from replication stress conditions, replication timing advances can be inherited by the next cellular generation, suggesting a new mechanism by which some cancer cells would adapt to cellular or environmental stress.

2021-05-19 | GSE156618 | GEO

Replication timing for the replication fountains

Project description:This dataset includes replication timing of WT K562 cells and cells with or without 600 nM Aphidicolin treatment.

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Microarray gene expression in RKO cell line under low replication stress

Project description:RKO cells were treated with low doses of aphidicolin (0,2µM) that inhibit replicative DNA polymerases and induce a mild replication stress. Expression data were analysed on control cells (DMSO), 16h of treatment (t0) and after release in complete new culture medium of 13h (N+1) using microarray (affymetrix Clarion S) We used microarray to analyse the impact of low replication stress on gene expression comparing DMSO or aphidicolin-treated cells at the end of the treatment (t0) and in daughter cells released from the replication stress (N+1).

2021-05-19 | GSE156521 | GEO

scRepli-seq analysis of aphidicolin treated embryos

Project description:To analyze chromosome abnormalities of 8-cell embryos with/without aphidicolin treatment, we performed single cell replication sequencing (scRepli-seq). This submission is similar to our submission GSE226309.

2024-06-24 | GSE255456 | GEO

Bru-seq nascent RNA sequencing of human and mouse cells: correlation to replication timing and genome instability

Project description:Bru-seq nascent RNA sequencing (PubMed ID 23973811) was performed on two primary human fibroblast cell lines, mouse embryonic stem cells, and GM12878 human lymphoblastoid cells. Read data, which include both exon and intron signals, were used to identify transcription unit spans genome-wide, where a transcription unit is roughly correspondent to the longest expressed isoform of a gene. However, because algorithms were not constrained by annotated genes, transcription units need not and often do not correspond precisely to gene boundaries and include extragenic transcription. Transcription units were then compared to separate data sets that comprised induced copy number variants, common fragile sites, and Repli-seq replication timing. The objective was to discover the relationships between transcription unit span and size, local genomic instability, and replication timing. This GEO sample series provides the span and intensity of transcription units called genome-wide in the various samples. Correlations to genome stability and replication timing are provided in the associated manuscript. In addition, one human fibroblast line and the mouse embryonic stem cells had paired samples treated and untreated with low dose aphidicolin. Gene RPKM signal intensities are provided for these samples, although comparing these was not the principal objective of the study. Bru-seq single-read nascent RNA sequencing on human 090 fibroblasts +/- aphidicolin treatment, human UMHF1 fibroblasts (3 replicates), human GM12878 lymphoblastoid cells, and mouse embryonic stem cells+/- aphidicolin treatment.

2014-10-17 | E-GEOD-55862 | biostudies-arrayexpress

scRepli-seq analysis of aphidicolin treated embryos

Project description:scRepli-seq analysis of aphidicolin treated embryos

| PRJNA1075060 | ENA

Six Acinetobacter genomes

Project description:Six Acinetobacter genomes

| PRJEB35515 | ENA

Stenotrophomonas acidaminiphila strain:T0-18

Project description:Stenotrophomonas acidaminiphila strain:T0-18 Genome sequencing

| PRJNA563291 | ENA

Bru-seq nascent RNA sequencing of human and mouse cells: correlation to replication timing and genome instability

2014-10-17 | GSE55862 | GEO

Single cell sequencing of human RPE1 and BJ cells to identify copy number alterations and replication timing after treatments with aphidicolin or siRNA against Mus81

Project description:Single cell sequencing of human RPE1 and BJ cells to identify copy number alterations and replication timing after treatments with aphidicolin or siRNA against Mus81

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