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Transcription-mediated supercoiling regulates genome folding and loop formation

ABSTRACT: Transcription-mediated supercoiling regulates genome folding and loop formation

PROVIDER: PRJNA716693 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14050236.fastq.gz	Fastqsanger.gz
	SRR14050237.fastq.gz	Fastqsanger.gz
	SRR14050238.fastq.gz	Fastqsanger.gz
	SRR14050239.fastq.gz	Fastqsanger.gz
	SRR14055067_1.fastq.gz	Fastqsanger.gz

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Transcription-mediated supercoiling regulates genome folding and loop formation [ChIP-Seq]

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Transcription-mediated supercoiling regulates genome folding and loop formation [RNA-Seq]

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Transcription-mediated supercoiling regulates genome folding and loop formation [ChIP-Seq]

Project description:The chromatin fiber folds into loops, however the mechanisms controlling loop extrusion are still poorly understood. Using super-resolution microscopy, we visualized that loops in intact nuclei are formed by a scaffold of cohesin complexes from which the DNA protrudes. RNA polymerase II decorates the top of the loops and is physically segregated from cohesin. Augmented looping upon increased loading of cohesin on chromosomes causes disruption of Lamin at the nuclear rim and chromatin blending, a homogenous distribution of chromatin within the nucleus. Altering supercoiling via either transcription or topoisomerase inhibition counteracts chromatin blending, increases chromatin condensation, disrupts loop formation and leads to altered cohesin distribution and mobility on chromatin. Overall, negative supercoiling generated by transcription is an important regulator of loop formation in vivo.

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Transcription-mediated supercoiling regulates genome folding and loop formation.

Project description:The chromatin fiber folds into loops, but the mechanisms controlling loop extrusion are still poorly understood. Using super-resolution microscopy, we visualize that loops in intact nuclei are formed by a scaffold of cohesin complexes from which the DNA protrudes. RNA polymerase II decorates the top of the loops and is physically segregated from cohesin. Augmented looping upon increased loading of cohesin on chromosomes causes disruption of Lamin at the nuclear rim and chromatin blending, a homogeneous distribution of chromatin within the nucleus. Altering supercoiling via either transcription or topoisomerase inhibition counteracts chromatin blending, increases chromatin condensation, disrupts loop formation, and leads to altered cohesin distribution and mobility on chromatin. Overall, negative supercoiling generated by transcription is an important regulator of loop formation in vivo.

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Transcription-mediated supercoiling regulates genome folding and loop formation

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

2021-07-22 | GSE169492 | GEO

Type II topoisomerases shape multi-scale 3D chromatin folding in regions of positive supercoils

Project description:Type II topoisomerases (TOP2s) resolve torsional stress accumulated during various cellular processes and are enriched at chromatin loop anchors and TAD boundaries, where, when trapped, can lead to genomic instability promoting the formation of oncogenic fusions. Whether TOP2s relieve topological constraints at these positions and/or participate in 3D chromosome folding, remains unclear. Here, we combine 3D genomics, imaging and GapRUN, a method for the genome-wide profiling of positive supercoiling, to assess the role of TOP2s in shaping chromosome organization in human cells. Acute TOP2 depletion led to the emergence of new, large-scale contacts at the boundaries between active, positively supercoiled and lamina-associated domains. TOP2-dependent changes at the higher-order chromatin folding were accompanied by remodeling of chromatin-nuclear lamina interactions and of gene expression, while at the chromatin loop level, TOP2 depletion predominantly remodeled transcriptionally-anchored, positively supercoiled loops. We propose that TOP2s act as a fine-regulator of chromosome folding at multiple scales.

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