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Cohesin-dependent chromosome loop extrusion is limited by transcription and stalled replication forks [Hi-C]

ABSTRACT: Cohesin-dependent chromosome loop extrusion is limited by transcription and stalled replication forks [Hi-C]

PROVIDER: PRJNA680815 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13147962_1.fastq.gz	Fastqsanger.gz
	SRR13147962_2.fastq.gz	Fastqsanger.gz
	SRR13147963_1.fastq.gz	Fastqsanger.gz
	SRR13147963_2.fastq.gz	Fastqsanger.gz
	SRR13147964_1.fastq.gz	Fastqsanger.gz

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Cohesin-dependent chromosome loop extrusion is limited by transcription and stalled replication forks [RNA-seq]

Project description:Genome function depends on regulated chromosome folding, and loop extrusion by the protein complex cohesin is essential for this multilayered organization. The chromosomal positioning of cohesin is controlled by transcription, and the complex also localizes to stalled replication forks. However, the role of transcription and replication in chromosome looping remains unclear. Here, we show that reduction of chromosome-bound RNA polymerase weakens normal cohesin loop extrusion boundaries, allowing cohesin to form new long-range chromosome cis interactions. Stress response genes activated by transcription inhibition are also shown to act as new loop extrusion boundaries. Furthermore, cohesin loop extrusion during early S-phase is jointly controlled by transcription and replication units. Together, the results reveal that replication and transcription machineries are chromosome folding regulators that block the progression of loop-extruding cohesin, opening for new perspectives on cohesin’s roles in genome function and stability.

2022-06-15 | GSE191207 | GEO

Cohesin-dependent chromosome loop extrusion is limited by transcription and stalled replication forks [Hi-C]

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Cohesin-dependent chromosome loop extrusion is limited by transcription and stalled replication forks

Project description:Cohesin-dependent chromosome loop extrusion is limited by transcription and stalled replication forks

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Cohesin-dependent chromosome loop extrusion is limited by transcription and stalled replication forks [ChIP-seq]

Project description:Cohesin-dependent chromosome loop extrusion is limited by transcription and stalled replication forks [ChIP-seq]

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Cohesin-dependent chromosome loop extrusion is limited by transcription and stalled replication forks [RNA-seq]

Project description:Cohesin-dependent chromosome loop extrusion is limited by transcription and stalled replication forks [RNA-seq]

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Chromatin structure governs stalled replication fork processing and cohesin loading

Project description:The progression of replication forks (RFs) can be challenged by obstacles of endogenous or exogenous origin. Stalled forks need to be readily stabilized and restarted in order to prevent genomic instability. Replication fork restart requires the recruitment of multiple enzymes and involves different DNA transactions. The MRX (Mre11-Rad50-Xrs2) complex plays a central role in this process. It has been implicated in the nucleolytic degradation of nascent DNA and in the loading of cohesin at stalled forks. However, little is known on how these functions are regulated. Here we show that MRX structural features are predominant on the nuclease activity of Mre11 for DNA resection at stalled replication forks. This results raise the question of the mechanisms by which MRX promotes nascent strand resection. At DNA double strand breaks (DSB) MRX promotes the binding of the chromatin remodeler RSC, from which the activity is required for 5’ end resection. Interestingly, MRX mutants exhibit increased nucleosome occupancy at stalled replication forks. This result suggest that a dynamic chromatin structure promoted by MRX could be required for the processing of stalled replication forks. Strinkingly the absence of two histones modifiers Gcn5 and Set1 recapitulates the phenotype of MRX mutants both on chromatin structure and nascent strand resection at stalled forks even though they are dispensable for its recruitment. Since nucleosomes also represent obstacles for the loading of SMC complexes on DNA, it is coherent that we observed that cohesin is no longer recruited at stalled forks in gcn5 and set1, as in MRX mutants. Together our data suggest that the regulation of chromatin structure at stalled replication forks is essential for their processing and to promote genome stability.

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Cohesin-dependent chromosome loop extrusion is limited by transcription and stalled replication forks

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

2022-06-15 | GSE162194 | GEO

Universal dynamics of cohesin-mediated loop extrusion

Project description:Most animal genomes are partitioned into Topologically Associating Domains (TADs), created by cohesin-mediated loop extrusion and defined by convergently oriented CTCF sites. The dynamics of loop extrusion and its regulation remains poorly characterized in vivo. Here, we tracked TAD anchors in living human cells to visualize and quantify cohesin-dependent loop extrusion across multiple endogenous genomic regions. We show that TADs are dynamic structures whose anchors are brought in proximity about once per hour and for 6-19 min (~16% of the time). TADs are continuously subjected to extrusion by multiple cohesin complexes, extruding loops at ~0.1 kb/s. Remarkably, despite strong differences of Hi-C patterns between the chromatin regions, their dynamics is consistent with the same density, residence time and speed of cohesin. Our results suggest that TAD dynamics is governed primarily by CTCF site location and affinity, which allows genome-wide predictive models of cohesin-dependent interactions.

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Project description:Topological stress can cause replication forks to stall as they converge upon one another during termination of vertebrate DNA synthesis. However, replication forks ultimately overcome topological stress and complete DNA synthesis, suggesting that alternative mechanisms can overcome topological stress. We performed a proteomic analysis of converging replication forks that were stalled by topological stress induced by loss or inhibition of topoisomerase IIα (TOP2α). Plasmid DNA was replicated in mock- or TOP2α-depleted Xenopus egg extracts as previously described (Heintzman et al. 2019). In parallel, replication was performed in the presence of the TOP2 inhibitor ICRF-193 (‘TOP2-i’) as an alternate means of preventing TOP2 activity (Heintzman et al. 2019). Chromatinized plasmid DNA was recovered 18 minutes after the onset of DNA synthesis, when most forks have normally merged but are stalled when TOP2 activity is prevented (Heintzman et al. 2019). Chromatin-bound proteins were recovered (Larsen et al. 2019) then analyzed by chromatin mass spectrometry and quantified by label free quantification.

2023-02-21 | PXD031170 | Pride

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