Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA395426 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5860260.fastq.gz | Fastqsanger.gz | |||
| SRR5860261.fastq.gz | Fastqsanger.gz | |||
| SRR5860262.fastq.gz | Fastqsanger.gz | |||
| SRR5860257.fastq.gz | Fastqsanger.gz | |||
| SRR5860258.fastq.gz | Fastqsanger.gz |
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Project description:Down-regulation (DR) of PREP1 (aka PKNOX1) tumor suppressor induces H2Ax foci in human fibroblasts. Here we have analyzed the effect of PREP1 DR on DNA replication using cell cycle analysis, Repliseq, DNA combing, ChIP-seq, RNA-seq and immunofluorescence (IF). In human cells, PREP1 DR similarly affects both the rate of DNA replication and the progression of cells through the S phase. Genome wide, PREP1 DR induces late to early DNA replication shifts in normally late-replicated genomic regions amounting to 25% of the genome, in addition to unscheduled origins firing. A concomitant strong increase of unidirectional replication forks explains the appearance of DNA damage foci. The DNA target of PREP1 DR is the Lamin Associated DNA, in agreement with the simultaneous decrease of Lamin B1. Therefore PREP1 is a novel regulator of replication timing and Lamin B1 level, which ChIP-seq and RNA-seq data indicate as independent from its transcriptional activity. This activity must constitute the basis for its tumor suppression function.
2018-02-28 | GSE101774 | GEO
Project description:Down-regulation (DR) of PREP1 (aka PKNOX1) tumor suppressor induces H2Ax foci in human fibroblasts. Here we have analyzed the effect of PREP1 DR on DNA replication using cell cycle analysis, Repliseq, DNA combing, ChIP-seq, RNA-seq and immunofluorescence (IF). In human cells, PREP1 DR similarly affects both the rate of DNA replication and the progression of cells through the S phase. Genome wide, PREP1 DR induces late to early DNA replication shifts in normally late-replicated genomic regions amounting to 25% of the genome, in addition to unscheduled origins firing. A concomitant strong increase of unidirectional replication forks explains the appearance of DNA damage foci. The DNA target of PREP1 DR is the Lamin Associated DNA, in agreement with the simultaneous decrease of Lamin B1. Therefore PREP1 is a novel regulator of replication timing and Lamin B1 level, which ChIP-seq and RNA-seq data indicate as independent from its transcriptional activity. This activity must constitute the basis for its tumor suppression function.
2018-02-28 | GSE101773 | GEO
Project description:Down-regulation (DR) of PREP1 (aka PKNOX1) tumor suppressor induces H2Ax foci in human fibroblasts. Here we have analyzed the effect of PREP1 DR on DNA replication using cell cycle analysis, Repliseq, DNA combing, ChIP-seq, RNA-seq and immunofluorescence (IF). In human cells, PREP1 DR similarly affects both the rate of DNA replication and the progression of cells through the S phase. Genome wide, PREP1 DR induces late to early DNA replication shifts in normally late-replicated genomic regions amounting to 25% of the genome, in addition to unscheduled origins firing. A concomitant strong increase of unidirectional replication forks explains the appearance of DNA damage foci. The DNA target of PREP1 DR is the Lamin Associated DNA, in agreement with the simultaneous decrease of Lamin B1. Therefore PREP1 is a novel regulator of replication timing and Lamin B1 level, which ChIP-seq and RNA-seq data indicate as independent from its transcriptional activity. This activity must constitute the basis for its tumor suppression function.
2018-02-28 | GSE101775 | GEO
Project description:PREP1 down-regulation changes the DNA replication timing of Lamin-associated DNA and induces DNA damage
| PRJNA395422 | ENA
Project description:PREP1 down-regulation changes the DNA replication timing of Lamin-associated DNA and induces DNA damage [ChIP-Seq]
| PRJNA395427 | ENA
Project description:PREP1 down-regulation changes the DNA replication timing of Lamin-associated DNA and induces DNA damage [Repli-Seq]
| PRJNA395425 | ENA
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
Project description:Multiple epigenetic pathways underlie the temporal order of DNA replication (replication timing) in the context of development and disease. DNA methylation by DNA methyltransferases (DNMTs) and downstream chromatin reorganization and transcriptional changes are thought to impact DNA replication, yet this remains to be comprehensively tested. Using cell biological and genome-wide approaches to measure replication timing, we identified a number of genomic regions undergoing subtle but reproducible replication timing changes in various DNMT-mutant mouse ES cell lines that include a line with a drug-inducible DNMT3a2 expression system. Replication timing within pericentromeric heterochromatin (PH) correlates with redistribution of H3K27me3 induced upon DNA hypomethylation: later replicating PH coincides with H3K27me3 enriched regions. In contrast, this relationship with H3K27me3 was not evident at chromosomal arm regions that undergo either early-to-late (EtoL) or late-to-early (LtoE) replication timing switching upon loss of DNMTs. Interestingly, transcriptional up- and down-regulation frequently coincide with earlier and later shifts in replication timing of chromosomal arm regions, respectively. Our study revealed previously unrecognized complex and diverse roles of DNMTs in shaping the mammalian DNA replication landscape.
2021-02-12 | GSE119405 | GEO
Project description:In multicellular organisms, developmental changes to replication timing occur in 400- 800 kb domains across half the genome. While clear examples of epigenetic control of replication timing have been described, a role for DNA sequence in mammalian replication timing has not been substantiated. To assess the role of DNA sequences in directing these changes, we profiled replication timing in mice carrying a genetically rearranged Human Chromosome 21 [Hsa21]. In two distinct mouse cell types, Hsa21 sequences maintained human-specific replication timing, except at points of Hsa21 rearrangement. Changes in replication timing at rearrangements extended up to 900 kb and consistently reconciled with the wild-type replication pattern at developmental boundaries of replication-timing domains. Our results demonstrate DNA sequencedriven regulation of Hsa21 replication timing during development and provide evidence that mammalian chromosomes consist of multiple independent units of replication timing regulation.
2012-06-05 | GSE38472 | GEO
Project description:In multicellular organisms, developmental changes to replication timing occur in 400- 800 kb domains across half the genome. While clear examples of epigenetic control of replication timing have been described, a role for DNA sequence in mammalian replication timing has not been substantiated. To assess the role of DNA sequences in directing these changes, we profiled replication timing in mice carrying a genetically rearranged Human Chromosome 21 [Hsa21]. In two distinct mouse cell types, Hsa21 sequences maintained human-specific replication timing, except at points of Hsa21 rearrangement. Changes in replication timing at rearrangements extended up to 900 kb and consistently reconciled with the wild-type replication pattern at developmental boundaries of replication-timing domains. Our results demonstrate DNA sequencedriven regulation of Hsa21 replication timing during development and provide evidence that mammalian chromosomes consist of multiple independent units of replication timing regulation. Profile comparison of fibroblast and T-cell cultures from trans-chromosomic mice and human and mouse controls.
2012-06-04 | E-GEOD-38472 | biostudies-arrayexpress