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Genome wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE169620 | GEO | 2024/05/13

REPOSITORIES: GEO

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Genomewide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

Project description:DNA replication progression can be affected by the presence of physical barriers on the DNA, like the RNA Polymerases, leading to replication stress and DNA damage. Nonetheless, we do not know the overall influence of transcription on DNA replication progression. To characterize what happens at sites where DNA replication forks stall and pause, we establish a genome-wide approach to identify them. This approach uses multiple timepoints to identify replication fork/stalling hotspots as the replication progresses through the genome. These sites are typically associated with increased DNA damage, overlap with fragile sites and with breakpoints of rearrangements identified in cancers, but do not overlap with replication origins. Overlaying these sites with a genome-wide analysis of RNA Polymerase II transcription, we find that replication fork stalling/pausing sites inside genes are directly related to transcription progression and activity. We also find instances where transcription activity favors replication progression because reduces histone density, but also that slowing down transcription elongation slows down directly replication progression through genes. This would indicate that transcription and replication can coexist over the same regions. Importantly, rearrangements found in cancers overlapping transcription-replication collision sites are detected in non-transformed cells and increase following treatment with ATM and ATR inhibitors. Altogether, our findings highlight how transcription and replication overlap during S-phase, with both positive and negative consequences for replication fork progression and genome stability by the coexistence of these two processes.

2024-05-13 | GSE267038 | GEO

Genome wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

Project description:DNA replication progression can be affected by the presence of physical barriers on the DNA, like RNA Polymerases, leading to replication stress and DNA damage. To characterize what happens at sites where DNA replication forks stall and pause, we establish a genome-wide approach to identify them. This approach uses multiple timepoints during S-phase, to identify replication fork/stalling hotspots throughout the genome. These sites are typically associated with increased DNA damage, overlap with fragile sites and with breakpoints of rearrangements identified in cancers, but do not overlap with replication origins. Overlaying these sites with a genome-wide analysis of RNA Polymerase II transcription, we found that replication fork stalling/pausing sites inside genes are directly related to transcription progression and activity. This would support data that indicate that transcription and replication can coexist over the same regions. We found instances where transcription activity by reducing histone density favors replication progression through genes, but also found that slowing down transcription elongation slows down directly replication progression through genes. Importantly, rearrangements found in cancers at transcription-replication collision sites can be detected in non-transformed cells and increased following treatment with ATM and ATR inhibitors. Altogether, our findings highlight how transcription and replication overlap during S-phase, with both positive and negative consequences for replication fork progression and genome stability.

2024-05-13 | GSE169619 | GEO

Genome wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

2024-05-13 | GSE169596 | GEO

Genomewide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

Project description:Genomewide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

| PRJNA1109387 | ENA

Genome wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

Project description:Genome wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

| PRJNA717167 | ENA

Genome wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

Project description:Genome wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

| PRJNA717229 | ENA

Genome wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

Project description:Genome wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

| PRJNA717227 | ENA

Replication fork barriers: pausing for a break or stalling for time?

Project description:Defects in chromosome replication can lead to translocations that are thought to result from recombination events at stalled DNA replication forks. The progression of forks is controlled by an essential DNA helicase, which unwinds the parental duplex and can stall on encountering tight protein-DNA complexes. Such pause sites are hotspots for recombination and it has been proposed that stalled replisomes disassemble, leading to fork collapse. However, in both prokaryotes and eukaryotes it now seems that paused forks are surprisingly stable, so that DNA synthesis can resume without recombination if the barrier protein is removed. Recombination at stalled forks might require other events that occur after pausing, or might be dependent on features of the surrounding DNA sequence. These findings have important implications for our understanding of the regulation of genome stability in eukaryotic cells, in which pausing of forks is mediated by specific proteins that are associated with the replicative helicase.

| S-EPMC1852754 | biostudies-other

Replication stalling at unstable inverted repeats: interplay between DNA hairpins and fork stabilizing proteins.

Project description:DNA inverted repeats (IRs) are hotspots of genomic instability in both prokaryotes and eukaryotes. This feature is commonly attributed to their ability to fold into hairpin- or cruciform-like DNA structures interfering with DNA replication and other genetic processes. However, direct evidence that IRs are replication stall sites in vivo is currently lacking. Here, we show by 2D electrophoretic analysis of replication intermediates that replication forks stall at IRs in bacteria, yeast, and mammalian cells. We found that DNA hairpins, rather than DNA cruciforms, are responsible for the replication stalling by comparing the effects of specifically designed imperfect IRs with varying lengths of their central spacer. Finally, we report that yeast fork-stabilizing proteins, Tof1 and Mrc1, are required to counteract repeat-mediated replication stalling. We show that the function of the Tof1 protein at DNA structure-mediated stall sites is different from its previously described effect on protein-mediated replication fork barriers.

| S-EPMC2481305 | biostudies-literature

Replication fork stalling elicits chromatin compaction for the stability of stalling replication forks.

Project description:DNA replication forks in eukaryotic cells stall at a variety of replication barriers. Stalling forks require strict cellular regulations to prevent fork collapse. However, the mechanism underlying these cellular regulations is poorly understood. In this study, a cellular mechanism was uncovered that regulates chromatin structures to stabilize stalling forks. When replication forks stall, H2BK33, a newly identified acetylation site, is deacetylated and H3K9 trimethylated in the nucleosomes surrounding stalling forks, which results in chromatin compaction around forks. Acetylation-mimic H2BK33Q and its deacetylase clr6-1 mutations compromise this fork stalling-induced chromatin compaction, cause physical separation of replicative helicase and DNA polymerases, and significantly increase the frequency of stalling fork collapse. Furthermore, this fork stalling-induced H2BK33 deacetylation is independent of checkpoint. In summary, these results suggest that eukaryotic cells have developed a cellular mechanism that stabilizes stalling forks by targeting nucleosomes and inducing chromatin compaction around stalling forks. This mechanism is named the "Chromsfork" control: Chromatin Compaction Stabilizes Stalling Replication Forks.

| S-EPMC6642376 | biostudies-literature

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