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Dynamic bimodal changes in CpG and non-CpG methylation genome-wide upon CGGBP1 loss-of-function

ABSTRACT: By depleting CGGBP1 in normal human fibroblasts 1064Sk using lentiviral shmiR (non-targeting or targeting CGGBP1) and by performing genome-wide sequencing (on bisulfite converted genomic DNA from both samples) we show that both gain and loss of cytosine methylation occurs upon CGGBP1 depletion. This gain and loss of methylation is clustered, spatially overlapping at major functional genomic regions and transcends all three cytosine sequence contexts. We demonstrate that CGGBP1 regulates cytosine methylation genome-wide through cis and trans-acting mechanisms. Library preparation for sequencing has been described in PMID 25981527.

ORGANISM(S): Homo sapiens

PROVIDER: GSE99274 | GEO | 2018/06/15

REPOSITORIES: GEO

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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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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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