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

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

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE162194 | GEO | 2022/06/15

REPOSITORIES: GEO

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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]

2022-06-15 | GSE162193 | GEO

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

2022-06-15 | GSE161522 | GEO

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

| PRJNA680814 | ENA

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]

| PRJNA678640 | ENA

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]

| PRJNA790450 | ENA

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]

| PRJNA680815 | ENA

RFWD3-Dependent Ubiquitination of RPA Regulates Repair at Stalled Replication Forks.

Project description:We have used quantitative proteomics to profile ubiquitination in the DNA damage response (DDR). We demonstrate that RPA, which functions as a protein scaffold in the replication stress response, is multiply ubiquitinated upon replication fork stalling. Ubiquitination of RPA occurs on chromatin, involves sites outside its DNA binding channel, does not cause proteasomal degradation, and increases under conditions of fork collapse, suggesting a role in repair at stalled forks. We demonstrate that the E3 ligase RFWD3 mediates RPA ubiquitination. RFWD3 is necessary for replication fork restart, normal repair kinetics during replication stress, and homologous recombination (HR) at stalled replication forks. Mutational analysis suggests that multisite ubiquitination of the entire RPA complex is responsible for repair at stalled forks. Multisite protein group sumoylation is known to promote HR in yeast. Our findings reveal a similar requirement for multisite protein group ubiquitination during HR at stalled forks in mammalian cells.

| S-EPMC4609029 | biostudies-literature

Artemis-dependent DNA double-strand break formation at stalled replication forks.

Project description:Stalled replication forks undergo DNA double-strand breaks (DSBs) under certain conditions. However, the precise mechanism underlying DSB induction and the cellular response to persistent replication fork stalling are not fully understood. Here we show that, in response to hydroxyurea exposure, DSBs are generated in an Artemis nuclease-dependent manner following prolonged stalling with subsequent activation of the ataxia-telangiectasia mutated (ATM) signaling pathway. The kinase activity of the catalytic subunit of the DNA-dependent protein kinase, a prerequisite for stimulation of the endonuclease activity of Artemis, is also required for DSB generation and subsequent ATM activation. Our findings indicate a novel function of Artemis as a molecular switch that converts stalled replication forks harboring single-stranded gap DNA lesions into DSBs, thereby activating the ATM signaling pathway following prolonged replication fork stalling.

| S-EPMC7657233 | biostudies-literature

A mechanism of cohesin-dependent loop extrusion organizes zygotic genome architecture.

Project description:Fertilization triggers assembly of higher-order chromatin structure from a condensed maternal and a naïve paternal genome to generate a totipotent embryo. Chromatin loops and domains have been detected in mouse zygotes by single-nucleus Hi-C (snHi-C), but not bulk Hi-C. It is therefore unclear when and how embryonic chromatin conformations are assembled. Here, we investigated whether a mechanism of cohesin-dependent loop extrusion generates higher-order chromatin structures within the one-cell embryo. Using snHi-C of mouse knockout embryos, we demonstrate that the zygotic genome folds into loops and domains that critically depend on Scc1-cohesin and that are regulated in size and linear density by Wapl. Remarkably, we discovered distinct effects on maternal and paternal chromatin loop sizes, likely reflecting differences in loop extrusion dynamics and epigenetic reprogramming. Dynamic polymer models of chromosomes reproduce changes in snHi-C, suggesting a mechanism where cohesin locally compacts chromatin by active loop extrusion, whose processivity is controlled by Wapl. Our simulations and experimental data provide evidence that cohesin-dependent loop extrusion organizes mammalian genomes over multiple scales from the one-cell embryo onward.

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