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DNA methylation insulates exons from CTCF loops with nuclear speckles (ChiP-Seq)

ABSTRACT: DNA methylation insulates exons from CTCF loops with nuclear speckles (ChiP-Seq)

PROVIDER: PRJNA900264 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22257237_1.fastq.gz	Fastqsanger.gz
	SRR22257237_2.fastq.gz	Fastqsanger.gz
	SRR22257238_1.fastq.gz	Fastqsanger.gz
	SRR22257238_2.fastq.gz	Fastqsanger.gz
	SRR22257239_1.fastq.gz	Fastqsanger.gz

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DNA methylation insulates exons from CTCF loops with nuclear speckles

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DNA methylation insulates exons from CTCF loops with nuclear speckles (HiChIP)

Project description:CTCF is necessary for the formation and maintenance of many DNA loops and Topologically Associating Domains, but the genomic features that influence CTCF looping are incompletely understood. We characterized the downstream effects of treating cells with a DNMT1 inhibitor and acute depletion of nuclear speckles to study the factors that influence CTCF looping.

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DNA methylation insulates exons from CTCF loops with nuclear speckles

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

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Senescent cells cluster CTCF on nuclear speckles to sustain their splicing program [Chipmentation]

Project description:Senescence —the end-point of the replicative life span of normal cells— is characterized by a complex sequence of molecular and biochemical events. One of these is the dramatic reorganization of CTCF into large senescence-induced CTCF clusters (SICCs). However, the molecular determinants, genomic consequences, and functional purpose of SICCs remained unknown. Here, we combine super-resolution imaging, 3D genomics, and functional assays with computational modelling to address all aspects of SICC emergence. First, we used modelling and data from the overexpression of nuclear factors lost upon senescence entry to explain how changes in the nuclear environment allow for CTCF clustering. Second, we discovered that cells entering senescence repurpose SRRM2 —a key component of nuclear speckles— and BANF1 —a protein known to act as ‘molecular glue’ for chromosomes during mitosis— to cluster CTCF on the surface of speckles, while rewiring higher-order genome architecture. Last, we could show that SICCs are required for the faithful execution of the senescence splicing program as their disruption by SRRM2 or BANF1 depletion reverts splicing choices. Together, the senescence-specific clustering of CTCF on nuclear speckles is a new paradigm of a change in the biochemical environment of the nucleus being translated into its architectural reorganization to allow for the deployment of a splicing program driving homeostatic deregulation.

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