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CGGBP1 regulates chromatin barrier activity and CTCF occupancy at repeats

ABSTRACT: CGGBP1 regulates chromatin barrier activity and CTCF occupancy at repeats

PROVIDER: PRJNA531700 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8872190.fastq.gz	Fastqsanger.gz
	SRR8872191.fastq.gz	Fastqsanger.gz
	SRR8872194.fastq.gz	Fastqsanger.gz
	SRR8872185.fastq.gz	Fastqsanger.gz
	SRR8872186.fastq.gz	Fastqsanger.gz

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CGGBP1 regulates chromatin barrier activity and CTCF occupancy at repeats

Project description:To study the role of CGGBP1 in regulation of CTCF occupancy, we performed CTCF ChIP-seq in HEK293T cells with three different levels of CGGBP1: (i) endogenous levels of CGGBP1 (ii) CGGBP1 knockdown, and (iii) CGGBP1 overexpression. Here, we show that CTCF binds to repeats as well as canonical CTCF-motifs and CGGBP1 determines the CTCF occupancy preference for repeats over canonical CTCF-motif. By combining CTCF ChIP-seq with histone modifications ChIP-seq (for H3K4me3, H3K9me3 and H3K27me3) under conditions of normal or CGGBP1 knockdown, we demonstrate that CTCF binding sites regulated by CGGBP1 correspond to chromatin barrier elements with profound effects on H3K9me3 distribution. In conclusion, these finding shows that CGGBP1 is a regulator of CTCF occupancy and serve as a regulator of barrier functions of CTCF-binding sites.

2019-09-23 | GSE129548 | GEO

CGGBP1-dependent CTCF-binding sites restrict ectopic transcription

Project description:CGGBP1-dependent CTCF-binding sites identified in Patel et. al. 2019 [PMID 31547883] serve as barrier elements consistent with asymmetrical levels of H3K9me3 in the flanks and asymmetrical RNA levels at these sites in the genome. In this study we have characterised the function of such CGGBP1-depenedent CTCF binding sites which are usually repeat rich in nature. By cloning one such CTCF-binding site in an episomal system, we have studied the barrier activity of this CGGBP1-dependent CTCF-binding sites in the prsesnce and absence of CGGBP1 in HEK293T cells through various molecular assays and RNA-sequencing. Our results show that these sites act as barrier for the ectopic transcription as the depletion of CGGBP1 lead to starnd-specific bidirectional transcription as a result of loss of barrier activity concomitant with the loss of CTCF-binding. Further, analysing the RNA-seq revealed that weakly transcribed sites are flanked by the CTCF-binding at transcription start and end sites in the presence of CGGBP1. However, CGGBP1 depletion leads to loss of barrier activity maintained by CGGBP1 with dispersed CTCF binding and a loss of transcription restriction. Such CGGBP1-dependent CTCF-binding sites prevents ectopic transcription.

2022-01-06 | GSE171990 | GEO

CGGBP1 regulates CTCF occupancy at repeats.

Project description:BACKGROUND:CGGBP1 is a repeat-binding protein with diverse functions in the regulation of gene expression, cytosine methylation, repeat silencing and genomic integrity. CGGBP1 has also been identified as a cooperator of histone-modifying enzymes and as a component of CTCF-containing complexes that regulate the enhancer-promoter looping. CGGBP1-CTCF cross talk in chromatin regulation has been hitherto unknown. RESULTS:Here, we report that the occupancy of CTCF at repeats depends on CGGBP1. Using ChIP-sequencing for CTCF, we describe its occupancy at repetitive DNA. Our results show that endogenous level of CGGBP1 ensures CTCF occupancy preferentially on repeats over canonical CTCF motifs. By combining CTCF ChIP-sequencing results with ChIP sequencing for three different kinds of histone modifications (H3K4me3, H3K9me3 and H3K27me3), we show that the CGGBP1-dependent repeat-rich CTCF-binding sites regulate histone marks in flanking regions. CONCLUSION:CGGBP1 affects the pattern of CTCF occupancy. Our results posit CGGBP1 as a regulator of CTCF and its binding sites in interspersed repeats.

| S-EPMC6757366 | biostudies-literature

CGGBP1-regulated cytosine methylation at CTCF-binding motifs resists stochasticity

Project description:To study if regulation of cytosine methylation and CTCF occupancy are interdependent and governed by the levels of CGGBP1, we specifically pulled-down methylated cytosines and found that some transcription factor binding sites including that of CTCF held out against the cytosine methylation changes. The cytosine methylation at CTCF-binding repeat-free motifs show a non-stochastic depdendence on CGGBP1 and occur at sites that mark cytosine methylation transition boundaries. We also show that allelic imbalance dictates stochastic methylation changes due to CGGBP1 depletion.

2020-07-20 | GSE145300 | GEO

CGGBP1 inhibits cytosine methylation at repetitive DNA sequences

Project description:By depleting CGGBP1 in normal human fibroblasts and by performing genome-wide sequencing (with and without bisulfite conversion) we show that upon CGGBP1 depletion cytosine methylation increases significantly at repeat regions. Using Pacbio sequencing of Alu and LINE-1 repeats amplified genome-wide from bisulfite converted DNA, we further establish the cytosine methylation-inhibitory functions of CGGBP1.

2015-08-26 | GSE60784 | GEO

CGGBP1-dependent CTCF-binding sites restrict ectopic transcription

Project description:CGGBP1-dependent CTCF-binding sites restrict ectopic transcription

| PRJNA721628 | ENA

ChIP-seq: Analysis of CTCF occupancy in unaffected and DM1 patient lymphoblastoid cell lines.

Project description:We performed CTCF ChIP-seq to determine the extent of CTCF occupancy alterations in two DM1 patient lymphoblastoid cell lines (LCLs) compared to an unaffected control LCL. Our results show that there were no large-scale changes in CTCF occupancy in the DM1 patient cells either genome-wide or in a 2 Mb region centered around the expanded repeats of DMPK.

2020-04-07 | GSE148179 | GEO

The CGG triplet repeat binding protein 1 counteracts DNA secondary structure formation to prevent transcription-replication stress

Project description:Short tracts of trinucleotide repeats with less than 10 repeats are found frequently throughout the genome without any apparent negative impact on DNA replication fork progression or transcription elongation. CGG binding protein 1 (CGGBP1) binds to CGG triplet repeats and has been implicated in multiple cellular processes such as transcription, replication and DNA damage. Here, we show that CGGBP1 binds to human gene promoter sites with short CGG repeat tracts prone to G-quadruplex and R-loop secondary structure formation. Depletion of CGGBP1 in human cells leads to substantial transcriptomic changes which coincides with increased replication fork stalling and transcription-replication conflicts. Consistently, an episomal model locus as well as endogenous candidate genes containing short tracts of CGG repeats show R-loop accumulation and increased RNAPII chromatin occupancy in CGGBP1-depleted cells. Mass spectrometry identifies the DEAD-box helicase DDX41 as a specific interaction partner of CGGBP1, thereby providing mechanistic insight how CGGBP1 can counteract the formation of secondary DNA structures at CGG repeats. Together, our work shows that short trinucleotide repeats are a source of genome-destabilizing secondary structures and cells rely on specific DNA-binding factors to maintain proper transcription and replication progression at short trinucleotide repeats.

2025-10-20 | PXD045654 | Pride

CGGBP1-regulated cytosine methylation at CTCF-binding motifs resists stochasticity

Project description:CGGBP1-regulated cytosine methylation at CTCF-binding motifs resists stochasticity

| PRJNA606696 | ENA

The homeotherm-conserved protein CGGBP1 connects heat stress to chromosomal fusions

Project description:We report that heat stress induces chromosomal fusion events in cell culture. We describe the findings first using normal primary fibroblasts [Coriell Cell Repository GM02639] and subsequently apply it to a system of HEK293T stable lines called CT and KD [described in PMID 31547883]. The stable line CT stands for Control shRNA and KD stands for a knockdown of human CGGBP1 using specific shRNA [Origene Lentiviral system TL313955V]. Our results suggest that as measured by the frequency of chromosomal fusions, the CGGBP1 knockdown in KD, when compared to CT, imitates the effects of heat stress. Further, ChIP-sequencing for TP53BP1 show genome-wide misdirected repairs at repeat flanks in KD as compared to CT. We show that CGGBP1 depletion and heat give rise to chromosomal fusions due to overlapping mechanisms that involve misdirected repair in the flanks of repeats genome-wide.

2022-01-10 | GSE169435 | GEO

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