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

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

PROVIDER: PRJNA702745 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13736600.fastq.gz	Fastqsanger.gz
	SRR13736601.fastq.gz	Fastqsanger.gz
	SRR13736602.fastq.gz	Fastqsanger.gz
	SRR13736603.fastq.gz	Fastqsanger.gz
	SRR13736604.fastq.gz	Fastqsanger.gz

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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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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.

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Local chromatin fiber folding represses transcription and loop extrusion in quiescent cells

Project description:A longstanding hypothesis is that chromatin fiber folding mediated by interactions between nearby nucleosomes represses transcription. However, it has been difficult to determine the relationship between local chromatin fiber compaction and transcription in cells. Further, global changes in fiber diameters have not been observed, even between interphase and mitotic chromosomes. We show that an increase in the range of local inter-nucleosomal contacts in quiescent yeast drives the compaction of chromatin fibers genome-wide. Unlike actively dividing cells, inter-nucleosomal interactions in quiescent cells require a basic patch in the histone H4 tail. This quiescence-specific fiber folding globally represses transcription and inhibits chromatin loop extrusion by condensin. These results reveal that global changes in chromatin fiber compaction can occur during cell state transitions, and establish physiological roles for local chromatin fiber folding in regulating transcription and chromatin domain formation.

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Chromatin Fiber Folding Represses Transcription and Loop Extrusion in Quiescent Cells

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

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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.

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