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A CpG island-encoded mechanism protects genes from premature transcription termination

ABSTRACT: A CpG island-encoded mechanism protects genes from premature transcription termination

PROVIDER: PRJNA821511 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18542300_1.fastq.gz	Fastqsanger.gz
	SRR18542300_2.fastq.gz	Fastqsanger.gz
	SRR18542301_1.fastq.gz	Fastqsanger.gz
	SRR18542301_2.fastq.gz	Fastqsanger.gz
	SRR18542302_1.fastq.gz	Fastqsanger.gz

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Project description:Transcription must be highly controlled to regulate gene expression and development. However, our understanding of the molecular mechanisms that influence transcription and how these are coordinated in cells to ensure normal gene expression remains rudimentary. Here, we reveal that actively transcribed CpG island-associated gene promoters recruit SET1 chromatin modifying complexes to enable gene expression. Counterintuitively, this effect is independent of SET1 complex histone modifying activity, and instead relies on the capacity of these complexes to interact with the RNA Polymerase II-binding protein, WDR82. Unexpectedly, we discover that SET1 complexes sustain gene transcription by counteracting the activity of the ZC3H4/WDR82 protein complex, which we show can pervasively terminate both genic and extragenic transcription. Therefore, we discover a new gene regulatory mechanism whereby CpG island elements nucleate a protein complex that protects genic transcription from premature termination, effectively distinguishing genic from non-genic transcription to enable gene expression.

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

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An evolutionarily conserved DNA-encoded logic shapes CpG island formation

Project description:An evolutionarily conserved DNA-encoded logic shapes CpG island formation

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An evolutionarily conserved DNA-encoded logic shapes CpG island formation

Project description:DNA methylation is an epigenetic modification of the vertebrate genome that contributes to transcriptional repression, imprinting, and X-chromosome inactivation. While the majority of the genome is blanketed in DNA methylation, regions known as CpG islands (CGIs) remain remarkably refractory to this modification. CpG islands are associated with roughly two thirds of gene promoters, are evolutionarily conserved, and play central roles in gene regulation, yet how they are protected from DNA methylation remains enigmatic. Based on the conserved nature of CpG islands, we have exploited genomic approaches and a transchromosomic model system to ask if DNA sequence is sufficient to specify the hypomethylated state at CpG islands when a human chromosome is newly introduced into mouse. Interestingly, this approach revealed that promoter-associated CGIs remain immensely refractory to DNA methylation regardless of the host species, in fitting with their conservation across vertebrate species and revealing that DNA sequence is a central driver in this outcome. In contrast, the methylation state of distal elements is highly variable between species and is host nucleus dependent. These alterations in methylation state at distal elements are defined by DNA nucleotide frequency and occupancy of DNA binding transcription factors, uncovering a widespread role for these features in defining the how this aspect of the epigenome forms away from gene promoters. These central principles are further supported by transplantation of mouse DNA sequences into the evolutionarily distant zebrafish genome, revealing the existence of a highly conserved and DNA encoded logic that shapes the vertebrate epigenome.

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