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Chromatin Fiber Folding Represses Transcription and Loop Extrusion in Quiescent Cells (ChIP-Seq)

ABSTRACT: Determining the conformation of chromatin in cells at the nucleosome level and its relationship to cellular processes has been a central challenge in biology. We show that in quiescent yeast, widespread transcriptional repression coincides with the local compaction of chromatin fibers into structures that are less condensed and more heteromorphic than canonical 30-nanometer forms. Acetylation or substitution of H4 tail residues decompacts fibers and leads to global transcriptional de-repression. Fiber decompaction also increases the rate of loop extrusion by condensin. These findings establish a role for H4 tail-dependent local chromatin fiber folding in regulating transcription and loop extrusion in cells. They also demonstrate the physiological relevance of canonical chromatin fiber folding mechanisms even in the absence of regular 30-nanometer structures.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE167017 | GEO | 2021/11/04

REPOSITORIES: GEO

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Chromatin Fiber Folding Represses Transcription and Loop Extrusion in Quiescent Cells (Micro-C XL)

Project description:Determining the conformation of chromatin in cells at the nucleosome level and its relationship to cellular processes has been a central challenge in biology. We show that in quiescent yeast, widespread transcriptional repression coincides with the local compaction of chromatin fibers into structures that are less condensed and more heteromorphic than canonical 30-nanometer forms. Acetylation or substitution of H4 tail residues decompacts fibers and leads to global transcriptional de-repression. Fiber decompaction also increases the rate of loop extrusion by condensin. These findings establish a role for H4 tail-dependent local chromatin fiber folding in regulating transcription and loop extrusion in cells. They also demonstrate the physiological relevance of canonical chromatin fiber folding mechanisms even in the absence of regular 30-nanometer structures.

2021-11-04 | GSE167019 | GEO

Chromatin Fiber Folding Represses Transcription and Loop Extrusion in Quiescent Cells

Project description:Chromatin Fiber Folding Represses Transcription and Loop Extrusion in Quiescent Cells

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Chromatin Fiber Folding Represses Transcription and Loop Extrusion in Quiescent Cells (ChIP-Seq)

Project description:Chromatin Fiber Folding Represses Transcription and Loop Extrusion in Quiescent Cells (ChIP-Seq)

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Resolving the 3D landscape of transcription-linked mammalian chromatin folding

Project description:Whereas folding of mammalian genomes at the large scale of epigenomic compartments and topologically associating domains (TADs) is now relatively well-understood, how chromatin is folded below this scale remains largely unexplored in mammals. Here, we overcome this limitation using a high-resolution 3C-based method, Micro-C, and probe the links between 3D-genome organization and transcriptional regulation in mouse stem cells. Combinatorial binding of transcription factors, cofactors, and chromatin modifiers spatially segregate TAD regions into various finer-scale structures with distinct regulatory features (i.e. stripes, dots, and domains linking promoter-promoter (P-P) or enhancer-promoter (E-P), and bundle contacts between Polycomb regions). E-P stripes extending from the edge of domains predominantly link co-expressed loci, often independently of CTCF and cohesin occupancy. Acute inhibition of transcription disrupts the gene-related folding features without altering higher-order chromatin structures. Analysis of ligation events sheds light on both the putative loop extrusion model and the “two-start” zig-zag 30-nanometer model of the chromatin fiber. Our work uncovers the finer-scale genome organization that establishes novel functional links between chromatin folding and gene regulation.

2019-05-21 | GSE130275 | GEO

Chromatin Fiber Folding Represses Transcription and Loop Extrusion in Quiescent Cells (Micro-C XL)

Project description:Chromatin Fiber Folding Represses Transcription and Loop Extrusion in Quiescent Cells (Micro-C XL)

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Chromatin extrusion explains key features of loop and domain formation in wild-type and engineered genomes

Project description:We recently used in situ Hi-C to create kilobase-resolution 3D maps of mammalian genomes. Here, we combine these with new Hi-C, microscopy, and genome-editing experiments to study the physical structure of chromatin fibers, domains, and loops. We find that the observed contact domains are inconsistent with the equilibrium state for an ordinary condensed polymer. Combining Hi-C data and novel mathematical theorems, we show that contact domains are also not consistent with a fractal globule. Instead, we use physical simulations to study two models of genome folding. In one, intermonomer attraction during polymer condensation leads to formation of an anisotropic "tension globule." In the other, CTCF and cohesin act together to extrude loops during interphase. Both models are consistent with the observed contact domains and with the observation that contact domains tend to form inside loops. However, the extrusion model explains a far wider array of observations, such as why loops tend not to overlap and why the CTCF-binding motifs at pairs of loop anchors lie in the convergent orientation. Finally, we perform 13 genome-editing experiments examining the effect of altering CTCF-binding sites on chromatin folding. The convergent rule correctly predicts the affected loop in every case. Moreover, the extrusion model accurately predicts in silico the 3D maps resulting from each experiment using only the location of CTCF-binding sites in the WT. Thus, we show that it is possible to disrupt, restore, and move loops and domains using targeted mutations as small as a single base pair. in situ Hi-C and HYbrid Capture Hi-C (Hi-C2) were used to probe the three-dimensional structure of the genome in two different human cell types before and after genome editing.

2015-10-23 | E-GEOD-74072 | biostudies-arrayexpress

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

Sensitivity of cohesin-chromatin association to high salt treatment corroborates non-topological mode of loop extrusion

Project description:Cohesin is a key organizer of chromatin folding in eukaryotic cells. Two basic activities of this ring-shaped protein complex are maintenance of sister chromatid cohesion and establishment of long-range DNA-DNA interactions through the process of loop extrusion. Though basic principles of both cohesion and loop extrusion have been described we still do not understand several crucial mechanistic details. One of such unresolved issues is the question of whether a cohesin ring topologically embraces DNA string(s) during loop extrusion. Here we show that cohesin complexes residing on CTCF-occupied genomic sites in mammalian cells do not interact with DNA topologically. We assessed stability of cohesin-dependent loops and cohesin association with chromatin in high ionic strength conditions in G1-synchronised HeLa cells. We found that increased salt concentration completely displaces cohesin from those genomic regions which correspond to CTCF-defined loop anchors. Unsurprisingly, CTCF-anchored cohesin loops also dissipate in these conditions. As topologically-engaged cohesin is considered to be salt-resistant, our data corroborate a non-topological model of loop extrusion.

2021-07-20 | GSE166387 | GEO

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