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

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

PROVIDER: PRJNA680814 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13065958.fastq.gz	Fastqsanger.gz
	SRR13065959.fastq.gz	Fastqsanger.gz
	SRR13065960.fastq.gz	Fastqsanger.gz
	SRR13065961.fastq.gz	Fastqsanger.gz
	SRR13065962.fastq.gz	Fastqsanger.gz

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

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.

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

Project description: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 [RNA-seq]

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

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