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Evidence that direct inhibition of transcription factor binding is the prevailing mode of gene and repeat repression by DNA methylation [RNA-Seq]

ABSTRACT: Evidence that direct inhibition of transcription factor binding is the prevailing mode of gene and repeat repression by DNA methylation [RNA-Seq]

PROVIDER: PRJNA764724 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15975000_1.fastq.gz	Fastqsanger.gz
	SRR15975000_2.fastq.gz	Fastqsanger.gz
	SRR15975001_1.fastq.gz	Fastqsanger.gz
	SRR15975001_2.fastq.gz	Fastqsanger.gz
	SRR15975002_1.fastq.gz	Fastqsanger.gz

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Evidence that direct inhibition of transcription factor binding is the prevailing mode of gene and repeat repression by DNA methylation

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Evidence that direct inhibition of transcription factor binding is the prevailing mode of gene and repeat repression by DNA methylation [RNA-Seq]

Project description:Cytosine methylation efficiently silences CpG-rich regulatory regions of genes and repeats in mammalian genomes. To what extent this entails direct inhibition of transcription factor (TF) binding versus indirect inhibition via recruitment of Methyl-CpG Binding Domain (MBD) proteins is unclear. Here we show that combinatorial genetic deletions of all four proteins with functional MBDs in mouse stem cells, derived neurons or a human cell line does not reactivate genes or repeats with methylated promoters. These do however become activated by methylation-restricted TFs if DNA methylation is removed. We identify several causal TFs in neurons, including ONECUT1, which is methylation-sensitive only at a motif variant. Rampantly upregulated retrotransposons in methylation-free neurons feature a CRE motif, which activates them in absence of DNA methylation via methylation-sensitive binding of CREB1. Our study reveals methylation-sensitive TFs in vivo and argues that direct inhibition, rather than indirect repression by the tested MBD proteins, is the prevailing mechanism of methylation-mediated repression at regulatory regions and repeats.

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Project description:Cytosine methylation efficiently silences CpG-rich regulatory regions of genes and repeats in mammalian genomes. To what extent this entails direct inhibition of transcription factor (TF) binding versus indirect inhibition via recruitment of methyl-CpG-binding domain (MBD) proteins is unclear. Here we show that combinatorial genetic deletions of all four proteins with functional MBDs in mouse embryonic stem cells, derived neurons or a human cell line do not reactivate genes or repeats with methylated promoters. These do, however, become activated by methylation-restricted TFs if DNA methylation is removed. We identify several causal TFs in neurons, including ONECUT1, which is methylation sensitive only at a motif variant. Rampantly upregulated retrotransposons in methylation-free neurons feature a CRE motif, which activates them in the absence of DNA methylation via methylation-sensitive binding of CREB1. Our study reveals methylation-sensitive TFs in vivo and argues that direct inhibition, rather than indirect repression by the tested MBD proteins, is the prevailing mechanism of methylation-mediated repression at regulatory regions and repeats.

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Evidence that direct inhibition of transcription factor binding is the prevailing mode of gene and repeat repression by DNA methylation

Project description:This SuperSeries is composed of the SubSeries listed below.

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