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Chromatin-bound RB targets promoters, enhancers, and CTCF-bound loci.

ABSTRACT: Chromatin-bound RB targets promoters, enhancers, and CTCF-bound loci.

PROVIDER: PRJNA734617 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14713100.fastq.gz	Fastqsanger.gz
	SRR14713101.fastq.gz	Fastqsanger.gz
	SRR14713102.fastq.gz	Fastqsanger.gz
	SRR14713103.fastq.gz	Fastqsanger.gz
	SRR14713104.fastq.gz	Fastqsanger.gz

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Chromatin-bound RB targets promoters, enhancers, and CTCF-bound loci.

Project description:RB’s interaction with chromatin is key to understanding its molecular functions. Using a novel ChIP-sequencing protocol, we identify the precise chromatin loci bound by various forms of human RB. RB targets three fundamentally different types of loci (promoters, enhancers, CTCF-sites), that are largely distinguishable by the mutually exclusive presence of E2F1, c-JUN and CTCF. E2F/DP facilitates RB association with promoters, whereas AP-1 recruits RB to enhancers. RB’s association with promoters and enhancers fluctuates: G1-arrest enriched RB at promoters, while S-phase progression redistributed RB towards enhancers. RB binding to RB/CTCF sites was unaltered by cell cycle progression. RB-bound promoters include the classic E2F targets and are similar between cell types. However, RB-bound enhancers are associated with different gene categories, including, notably, MAPK signaling, and they vary between cell types. We propose that RB has a well-preserved role controlling E2F in G1, and cell type-specific effects at enhancers when cells enter S-phase.

2022-08-01 | GSE176035 | GEO

Chromatin-bound RB targets promoters, enhancers, and CTCF-bound loci and is redistributed by cell-cycle progression.

Project description:The interaction of RB with chromatin is key to understanding its molecular functions. Here, for first time, we identify the full spectrum of chromatin-bound RB. Rather than exclusively binding promoters, as is often described, RB targets three fundamentally different types of loci (promoters, enhancers, and insulators), which are largely distinguishable by the mutually exclusive presence of E2F1, c-Jun, and CTCF. While E2F/DP facilitates RB association with promoters, AP-1 recruits RB to enhancers. Although phosphorylation in CDK sites is often portrayed as releasing RB from chromatin, we show that the cell cycle redistributes RB so that it enriches at promoters in G1 and at non-promoter sites in cycling cells. RB-bound promoters include the classic E2F-targets and are similar between lineages, but RB-bound enhancers associate with different categories of genes and vary between cell types. Thus, RB has a well-preserved role controlling E2F in G1, and it targets cell-type-specific enhancers and CTCF sites when cells enter S-phase.

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Myeloid leukemia dependency MYNRL15 exemplifies class of CTCF-bound lncRNA loci

Project description:Myeloid leukemia dependency MYNRL15 exemplifies class of CTCF-bound lncRNA loci

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Myeloid leukemia dependency MYNRL15 exemplifies class of CTCF-bound lncRNA loci [CUT&RUN]

Project description:Myeloid leukemia dependency MYNRL15 exemplifies class of CTCF-bound lncRNA loci [CUT&RUN]

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Myeloid leukemia dependency MYNRL15 exemplifies class of CTCF-bound lncRNA loci [ATAC-Seq]

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Myeloid leukemia dependency MYNRL15 exemplifies class of CTCF-bound lncRNA loci [RNA-Seq]

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ZNF143 mediates CTCF-bound promoter-enhancer loops required for murine hematopoietic stem and progenitor cell function

Project description:CCCTC binding factor (CTCF) is an important factor in the maintenance of chromatin chromatin interactions, yet the mechanism regulating its binding to chromatin is unknown. We demonstrate that zinc finger protein 143 (ZNF143) is a key regulator for CTCF bound promoter enhancer loops. In the murine genome, a large percentage of CTCF and ZNF143 DNA binding motifs are distributed 37 bp apart in the convergent orientation. Furthermore, deletion of ZNF143 leads to loss of CTCF binding on promoter and enhancer regions associated with gene expression changes. CTCF bound promoter enhancer loops are also disrupted after excision of ZNF143. ZNF143 CTCF bound promoter enhancer loops regulate gene expression patterns essential for maintenance of murine hematopoietic stem and progenitor cell integrity. Our data suggest a common feature of gene regulation that ZNF143 is a critical factor for CTCF bound promoter enhancer loops.

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ERCC1-XPF Cooperates with CTCF and the Cohesin to Facilitate the Developmental Silencing of Imprinted Genes

Project description:Inborn defects in DNA repairare associated with complex developmental disorders whose causal mechanisms are poorly understood. Using an in vivo biotinylation tagging approach in mice, we show that the nucleotide excision repair (NER) structure-specific endonuclease ERCC1-XPF complex interacts with the insulator binding protein CTCF, the cohesin subunits SMC1A and SMC3 and with MBD2; the factors co-localize with ATRX at the promoters and control regions (ICRs) of imprinted genes during postnatal hepatic development. Loss of Ercc1or exposure to mitomycin C triggers the localization of CTCF to heterochromatin, the dissociation of the CTCF-cohesin complex and ATRXfrom promoters and ICRs,altered histone marks and the aberrant developmental expression of imprinted genes without altering DNA methylation. We propose that ERCC1-XPF cooperates with CTCF and the cohesinto facilitatet he developmental silencing of imprinted genes and that persistent DNA damage triggers chromatin changes that affect gene expression programs associated with NER disorders.

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CTCF blocks anti-sense transcription initiation at divergent gene promoters [ChIP-Seq]

Project description:Transcription is typically divergent, initiating at closely spaced oppositely oriented core promoters to produce sense and unstable upstream antisense transcripts (uasTrx). How antisense transcription is regulated and coordinated with sense transcription is largely unknown. Here by combining acute degradation of the multi-functional transcription factor CTCF and nascent transcription measurements, we find that CTCF specifically suppresses antisense but not sense transcription at hundreds of divergent promoters, the great majority of which bear proximal CTCF binding sites. Genome editing, chromatin conformation studies and 5’ transcript mapping revealed that CTCF directly suppresses uasTrx initiation in manner independent of its chromatin architectural function. Primary transcript RNA FISH revealed co-bursting of sense and anti-sense transcripts is disfavored, suggesting CTCF-regulated competition for transcription initiation. In sum, CTCF shapes the noncoding transcriptional landscape by suppressing upstream antisense transcription.

2022-05-02 | GSE173443 | GEO

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