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The amniote-conserved DNA-binding domain of CGGBP1 restricts cytosine methylation of transcription factor binding sites in proximal promoters to regulate gene expression

ABSTRACT: The amniote-conserved DNA-binding domain of CGGBP1 restricts cytosine methylation of transcription factor binding sites in proximal promoters to regulate gene expression

PROVIDER: PRJNA1123167 | ENA |

REPOSITORIES: ENA

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The amniote-conserved DNA-binding domain of CGGBP1 restricts cytosine methylation of transcription factor binding sites in proximal promoters to regulate gene expression (HTS)

Project description:Truncated forms of CGGBP1 with (N-term) or without (C-term) the DNA-binding domain (DBD) have been used to to assay global cytosine methylation. HEK293T cells with endogenous CGGBP1 knocked down were used to over-express truncated forms of CGGBP1 followed by MeDIP-Seq analysis. Genome-wide analyses of cytosine methylation and binding of CGGBP1 DBD show that CGGBP1 restricts cytosine methylation in a manner that depends on its DBD and its DNA-binding. Our findings suggest that CGGBP1 protects transcription factor binding sites (TFBS) from cytosine methylation-associated loss. A superimposition of our results and evolution of CGGBP1 suggests that mitigation of cytosine methylation is majorly achieved by its N-terminal DBD. Our results position CGGBP1 DNA-binding as a major evolutionarily acquired mechanism through which it keeps cytosine methylation under check and regulates TFBS retention.

2024-11-17 | GSE269791 | GEO

The amniote-conserved DNA-binding domain of CGGBP1 restricts cytosine methylation of transcription factor binding sites in proximal promoters to regulate gene expression

Project description:Truncated forms of CGGBP1 with (N-term) or without (C-term) the DNA-binding domain (DBD) have been used to to assay global gene expression. HEK293T cells with endogenous CGGBP1 knocked down were used to over-express truncated forms of CGGBP1 followed by RNA extraction and one-coloured global gene expression analysis. The data suggests that while the C-term of CGGBP1 is the major repressor of transcription, just the N-term containing the DBD fails to achieve so. Proximal promoters of CGGBP1-repressed genes, although significantly GC-poor, contain GC-rich transcription factor binding motifs and exhibit base compositions indicative of low C-T transition rates due to targeted prevention of cytosine methylation. Our findings suggest that CGGBP1 protects transcription factor binding sites (TFBS) from cytosine methylation-associated loss and thereby regulates gene expression. By analysing orthologous promoter sequences, we show that protection from cytosine methylation is a function of CGGBP1 progressively acquired during vertebrate evolution.

2024-11-17 | GSE269654 | GEO

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 from higher amniotes restricts cytosine methylation and drives a GC-bias in transcription factor binding sites at repressed promoters [MeDIP-Seq]

Project description:Human CGGBP1 has been attributed multiple function related to the regulation of gene expression, cytosine methylation (including non-CpG methylation), related epigenetic states of target gene promoter regions and somatic mutation rates. CGGBP1 has also been shown to be a prominent transcription repressor of protein coding genes as well as repetitive elements, mainly Alu-SINEs. There is a possibility that CGGBP1-regulated cytosine methylation affects base mutation rates (C-T transitions) thereby directing TFBS evolution in the human genome. Some recent data suggest that the DNA-binding activity of human CGGBP1 prevents TFBS from cytosine methylation and preserves their GC content. The DNA-binding domain of CGGBP1 is conserved more than its other segments which contain no identifiable domains. In this study we assay global cytosine methylation using MeDIP-seq on human cells (HEK293T) over-expressing only representative vertebrate species (Latimeria chalumnae (Lc), Anolis carolinenesis (Ac), Gallus gallus (Gg), Homo sapiens (Hs)) and perform comparative analyses. Our analyses encompass a parallel global expression profiling (using Agilent arrays, submitted separately to NCBI GEO) and a large-scale estimation of TFBS C-T transition mutation rates from orthologs of genes repressed by the various forms of CGGBP1 used in this study. We report that cytosine methylation restriction by CGGBP1 promotes GC retention in some GC-rich TFBSs.

2025-07-31 | GSE281704 | GEO

The amniote-conserved DNA-binding domain of CGGBP1 restricts cytosine methylation of transcription factor binding sites in proximal promoters to regulate gene expression (HTS)

Project description:The amniote-conserved DNA-binding domain of CGGBP1 restricts cytosine methylation of transcription factor binding sites in proximal promoters to regulate gene expression (HTS)

| PRJNA1123700 | ENA

CGGBP1 from higher amniotes restricts cytosine methylation and drives a GC-bias in transcription factor binding sites at repressed promoters [Array]

Project description:Human and other vertebrate representative forms of CGGBP1 have been used in this study to assay global gene expression. HEK293T cells with endogenous CGGBP1 knocked down were used to over-express other vertebrate representative forms of CGGBP1 (Latimeria chalumnae (Lc), Anolis carolinensis (Ac), Gallus gallus (Gg)) followed by RNA extraction and one-coloured global gene expression analysis (Agilent). HEK293T cells with normal level of endogenous CGGBP1 were used to over-express Human CGGBP1 (Hs) or pcDNA3.1(+) empty vector (Ev). Overexpression of CGGBP1 forms resulted in the repression of specific gene sets at two different temperatures (37 degrees and 40 degrees Celsius). The proximal promoters of these repressed genes exhibit a marked difference in the occurrence of GC-rich transcription factor binding sites (TFBSs). Through additional studies on these samples we have separately assayed global cytosine methylation patterns (submitted separately to NCBI GEO) and reported that the GC content of these promoters is determined by a combination of motif occurrence as well as motif GC contents. Notably, the within these gene promoters human CGGBP1 was found to restrict cytosine methylation at certain GC-rich TFBSs. A high-throughput analysis of the GC compositional bias across these CGGBP1-regulated TFBSs, using orthologous sequences from over 100 species, revealed a strong link between CGGBP1-induced cytosine methylation restriction and GC retention at specific TFBSs. Further, orthology analysis showed that this regulatory mechanism of CGGBP1 is conserved in higher amniotes (birds and mammals) and exhibits lineage-specific variations in lower amniotes (reptiles).

2025-07-31 | GSE281705 | 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-regulated cytosine methylation at CTCF-binding motifs resists stochasticity

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

| PRJNA606696 | ENA

CGGBP1 from higher amniotes restricts cytosine methylation and drives a GC-bias in transcription factor binding sites at repressed promoters [Array]

Project description:CGGBP1 from higher amniotes restricts cytosine methylation and drives a GC-bias in transcription factor binding sites at repressed promoters [Array]

| PRJNA1185260 | ENA

The amniote-conserved DNA-binding domain of CGGBP1 restricts cytosine methylation of transcription factor binding sites in proximal promoters to regulate gene expression.

Project description:CGGBP1 is a GC-rich DNA-binding protein which is important for genomic integrity, gene expression and epigenome maintenance through regulation of CTCF occupancy and cytosine methylation. It has remained unclear how CGGBP1 integrates multiple diverse functions with its simple architecture of only a DNA-binding domain tethered to a C-terminal tail with low structural rigidity. We have used truncated forms of CGGBP1 with or without the DNA-binding domain (DBD) to assay cytosine methylation and global gene expression. Proximal promoters of CGGBP1-repressed genes, although significantly GC-poor, contain GC-rich transcription factor binding motifs and exhibit base compositions indicative of low C-T transition rates due to prevention of cytosine methylation. Genome-wide analyses of cytosine methylation and binding of CGGBP1 DBD show that CGGBP1 restricts cytosine methylation in a manner that depends on its DBD and its DNA-binding. The CGGBP1-repressed genes show an increase in promoter cytosine methylation alongside a decrease in transcript abundance when the DBD-deficient CGGBP1 is expressed. Our findings suggest that CGGBP1 protects transcription factor binding sites (TFBS) from cytosine methylation-associated loss and thereby regulates gene expression. By analysing orthologous promoter sequences we show that restriction of cytosine methylation is a function of CGGBP1 progressively acquired during vertebrate evolution. A superimposition of our results and evolution of CGGBP1 suggests that mitigation of cytosine methylation is majorly achieved by its N-terminal DBD. Our results position CGGBP1 DNA-binding as a major evolutionarily acquired mechanism through which it keeps cytosine methylation under check and regulates TFBS retention and gene activity.

| S-EPMC11575156 | biostudies-literature

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