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Constitutively bound CTCF sites maintain 3D chromatin architecture and long-range epigenetically regulated domains

ABSTRACT: Constitutively bound CTCF sites maintain 3D chromatin architecture and long-range epigenetically regulated domains

PROVIDER: PRJNA517606 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10152993_1.fastq.gz	Fastqsanger.gz
	SRR10152993_2.fastq.gz	Fastqsanger.gz
	SRR10152994_1.fastq.gz	Fastqsanger.gz
	SRR10152994_2.fastq.gz	Fastqsanger.gz
	SRR10152995_1.fastq.gz	Fastqsanger.gz

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Constitutively bound CTCF sites maintain 3D chromatin architecture and long-range epigenetically regulated domains.

Project description:The architectural protein CTCF is a mediator of chromatin conformation, but how CTCF binding to DNA is orchestrated to maintain long-range gene expression is poorly understood. Here we perform RNAi knockdown to reduce CTCF levels and reveal a shared subset of CTCF-bound sites are robustly resistant to protein depletion. The 'persistent' CTCF sites are enriched at domain boundaries and chromatin loops constitutive to all cell types. CRISPR-Cas9 deletion of 2 persistent CTCF sites at the boundary between a long-range epigenetically active (LREA) and silenced (LRES) region, within the Kallikrein (KLK) locus, results in concordant activation of all 8 KLK genes within the LRES region. CTCF genome-wide depletion results in alteration in Topologically Associating Domain (TAD) structure, including the merging of TADs, whereas TAD boundaries are not altered where persistent sites are maintained. We propose that the subset of essential CTCF sites are involved in cell-type constitutive, higher order chromatin architecture.

| S-EPMC6946690 | biostudies-literature

Constitutively bound CTCF sites maintain 3D chromatin architecture and long-range epigenetically regulated domains

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

2019-11-18 | GSE125641 | GEO

KDM4C epigenetically regulates and forms a feed-forward loop with ALDH1A3 to maintain gastric cancer stemness

Project description:Gastric cancer (GC) stem cells (GCSCs) are characterized as high level of ALDH activity, however, the mechanisms of maintenance of high ALDH activity and stemness in GCSCs are largely unknown. Here, we report that KDM4C, a H3K9me2/3-demethylase, epigenetically regulates ALDH1A3 by histone demethylation and forms a feed-forward loop with ALDH1A3 to supports GS stemness. Ectopic expression of both KDM4C and ALDH1A3 promotes the properties of GCSCs, including spherogenecity, self-renewal, CD44 expression and ALDH activity; knockdown of anyone abolished the effect of each other. KDM4C directly binds to the promoter of ALDH1A3, leads to histone demethylation, thereby promoting ALDH1A3 transcription. Upregulated ALDH1A3 in turn transcriptionally upregulates KDM4C. Simultaneous inhibition of KDM4C and ALDH1A3 synergistically sensitizes GC sphere-derived cells to traditional chemotherapeutic drugs. The finding that upregulated ALDH1A3 promotes its own transcription via KDM4C-mediated epigenetic modification represents an important feed-forward mechanism for GCSCs to maintain stemness and promote tumourigenesis and our work thus suggests a novel therapeutic strategy for eradicating human GCSCs. To investigate the mechanisms underlying KDM4C promoting CG stemness, we identified the differentially expressed proteins (DEPs) between KDM4C-overexpressing and control AGS cells by iTRAQ-based quantitative proteomic analysis.

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Constitutively Active Foxo3 in Oocytes Preserves Ovarian Reserve in Mice

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Constitutively Active Foxo3 in Oocytes Preserves Ovarian Reserve in Mice

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Constitutively Active YAP/TAZ Target Genes

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A distinct isoform of lymphoid enhancer binding factor 1 (LEF1) epigenetically restricts EBV reactivation to maintain viral latency

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The FUN30 Chromatin Remodeler Fft3 Protects Centromeric and Subtelomeric Domains from Euchromatin Formation

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2011-04-02 | E-MEXP-3044 | biostudies-arrayexpress

Expression analysis of Reh cells after transfection with constitutively active variants of IRF5 (IRF5-4D) and/or constitutively active IKKβ(EE)

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