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Diverse CGG binding proteins across eukaryotes produced by independent domestications of hAT transposons

ABSTRACT: The human transcription factor (TF) CGGBP1 (“CGG Binding Protein”) is conserved only in amniotes, and is believed to derive from the zf-BED and Hermes transposase DNA-binding domains (DBDs) of a hAT DNA transposon. Here, we examine the DNA binding preferences of a wide variety of metazoan CGGBP1-like TFs with this bipartite domain using PBM experiments. The derived motifs are available at ...

ORGANISM(S): Fundulus heteroclitus Erpetoichthys calabaricus Mola mola Locusta migratoria Amphiprion ocellaris Austrofundulus limnaeus Rhipicephalus appendiculatus Labeo rohita Rhodnius prolixus Anabarilius grahami Petromyzon marinus Aedes aegypti Chrysemys picta Salarias fasciatus Crocodylus porosus Homo sapiens Latimeria chalumnae Hippocampus comes Sphaeramia orbicularis Acyrthosiphon pisum Sparus aurata Salmo salar Rhizophagus irregularis Culex quinquefasciatus Kryptolebias marmoratus Nematostella vectensis synthetic construct Anabas testudineus Hofstenia miamia Gallus gallus Paramormyrops kingsleyae Acanthochromis polyacanthus Amphiprion percula Acipenser ruthenus Hucho hucho Cyprinus carpio

PROVIDER: GSE157085 | GEO | 2021/02/09

REPOSITORIES: GEO

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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 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

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

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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)

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2024-11-17 | GSE269791 | GEO

Diverse CGG binding proteins across eukaryotes produced by independent domestications of hAT transposons

Project description:Diverse CGG binding proteins across eukaryotes produced by independent domestications of hAT transposons

| PRJNA660048 | ENA

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

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2024-11-17 | GSE269654 | 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.

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Diverse Eukaryotic CGG-Binding Proteins Produced by Independent Domestications of hAT Transposons.

Project description: Not available

| S-EPMC8097297 | biostudies-literature

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.

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Growth signals employ CGGBP1 to suppress transcription of Alu-SINEs [ChIP-Seq]

Project description:Alu SINEs are the most numerous frequently occurring transcription units in our genomes 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. Examination of one DNA binding protein in two different conditions of treatment.

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