CGGBP1-dependent CTCF-binding sites restrict ectopic transcription
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ABSTRACT:
PROVIDER: PRJNA721628 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14228534_1.fastq.gz | Fastqsanger.gz | |||
| SRR14228535_1.fastq.gz | Fastqsanger.gz |
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Project description:CGGBP1-dependent CTCF-binding sites restrict ectopic transcription
| PRJNA721628 | ENA
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
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
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
Project description:CGGBP1-regulated cytosine methylation at CTCF-binding motifs resists stochasticity
| PRJNA606696 | ENA
Project description:CGGBP1 regulates chromatin barrier activity and CTCF occupancy at repeats
| PRJNA531700 | ENA
Project description:Pervasive usage of alternative promoters leads to deregulation of gene expression in carcinogenesis and may drive the emergence of new genes in spermatogenesis. However, little is known regarding the mechanisms underpinning the activation of alternative promoters. In our present study, we uncovered a novel mechanism by which alternative cancer-testis-specific transcription is activated from the intergenic and intronic clustered CTCF binding sites, which are transcriptionally inert in normal somatic cells. BORIS/CTCFL, a paralog of CTCF with cancer-testis-specific expression forms a heterodimer with CTCF at the clustered binding sites thus triggering epigenetic reprogramming of these sites into units of active transcription. BORIS binding to CTCF sites leads to the recruitment of chromatin-remodeling factor SRCAP, with subsequent replacement of H2A histone with H2A.Z, therefore creating a more relaxed chromatin state in the nucleosomes flanking the clustered binding sites. This facilitates opening of chromatin beyond CTCF/BORIS binding sites and paves the way to the recruitment of multiple additional transcription factors, thereby activating transcription from a given binding site. We demonstrate that the CTCF binding sites, epigenetically reprogrammed by ectopic BORIS expression can drive the expression of cancer-testis genes, long-noncoding RNAs, retro-pseudogenes, and dormant transposable elements harbored by activated long transcripts. Taking together, our results reveal that BORIS functions as a transcription factor that epigenetically reprograms clustered CTCF binding sites into transcriptional start sites, promoting transcription from alternative promoters in both germ cells and cancer cells.
2024-01-03 | GSE207058 | GEO
Project description:Alu SINEs are the most numerous frequently occurring transcription units in our genome and possess sequence competence for transcription by RNA Pol III. However, through poorly understood mechanisms, the Alu RNA levels are maintained at very low levels in normal somatic cells with obvious benefits of low rates of Alu retrotransposition and energy-economical deployment of RNA Pol III to the tRNA genes which share promoter structure and polymerase requirements with Alu SINEs. Using comparative ChIP sequencing, we unveil that a repeat binding protein, CGGBP1, binds to the transcriptional regulatory regions of Alu SINEs thereby impeding Alu transcription by inhibiting RNA Pol III recruitment. We show that this Alu-silencing depends on growth factor stimulation of cells and subsequent tyrosine phosphorylation of CGGBP1. Importantly, CGGBP1 ensures a sequence-specific discriminative inhibition of RNA Pol III activity at Alu promoters, while sparing the structurally similar tRNA promoters. Our data suggest that CGGBP1 contributes to growth-related transcription by preventing the hijacking of RNA Pol III by Alu SINEs. This study was used to find out the effect of CGGBP1 on serum-induced changes in gene expression and effect of serum on gene expression regulation by CGGBP1. Gene expression profiling of normal human fibroblasts under 4 different experimental perturbations: serum starvation or serum stimulation and CGGBP1 depletion or normal CGGBP1 levels.
2015-12-21 | E-GEOD-54058 | biostudies-arrayexpress
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
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