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Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment

ABSTRACT: Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment

PROVIDER: PRJNA1021513 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26190623_1.fastq.gz	Fastqsanger.gz
	SRR26190623_2.fastq.gz	Fastqsanger.gz
	SRR26190624_1.fastq.gz	Fastqsanger.gz
	SRR26190624_2.fastq.gz	Fastqsanger.gz
	SRR26190625_1.fastq.gz	Fastqsanger.gz

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Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment [RNA-seq]

Project description:How constitutive allelic methylation at imprinting control regions (ICRs) interacts with other levels of regulation to drive timely parental allele-specific expression along large imprinted domains remains partially understood at most imprinted loci. To gain insight into the regulation of the Peg13-KcnK9 domain, an imprinted domain with important brain functions, during neural commitment, we performed a detailed integrative analysis of the epigenetic, transcriptomic and cis-spatial organisation in an allele-specific manner in a mouse stem cell-based model of corticogenesis that recapitulates the control of imprinted gene expression in the embryonic brain. We have evidence that despite an allelic higher order chromatin structure associated with the paternally CTCF-bound Peg13 ICR, enhancer-Kcnk9 promoter contacts can occur on both alleles, although they are only productive on the maternal allele. This observation challenges the canonical model in which CTCF binding isolates the enhancer and its target gene on either side, and suggests a more nuanced role for allelic CTCF binding at the ICR of this locus.

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Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment [Cut&Run]

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Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment [ChIP-seq]

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Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment [4C-seq]

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Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment [ChIP-seq]

Project description:Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment [ChIP-seq]

| PRJNA1021518 | ENA

Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment [RNA-seq]

Project description:Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment [RNA-seq]

| PRJNA1021520 | ENA

Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment [Cut&Run]

Project description:Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment [Cut&Run]

| PRJNA1021519 | ENA

Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment [4C-seq]

Project description:Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment [4C-seq]

| PRJNA1021517 | ENA

Allelic chromatin structure primes imprinted expression of Kcnk9 during neurogenesis

Project description:Differences in chromatin state inherited from the parental gametes influence the regulation of maternal and paternal alleles in offspring. This phenomenon, known as genomic imprinting, results in genes preferentially transcribed from one parental allele. While local epigenetic factors such as DNA methylation are known to be important for the establishment of imprinted gene expression, less is known about the mechanisms by which differentially methylated regions (DMRs) lead to differences in allelic expression across broad stretches of chromatin. Allele-specific higher-order chromatin structure has been observed at multiple imprinted loci, consistent with the observation of allelic binding of the chromatin-organizing factor CTCF at multiple DMRs. However, whether allelic chromatin structure impacts allelic gene expression is not known for most imprinted loci. Here we characterize the mechanisms underlying brain-specific imprinted expression of the Peg13-Kcnk9 locus, an imprinted region associated with intellectual disability. We performed region capture Hi-C on mouse brain from reciprocal hybrid crosses and found imprinted higher-order chromatin structure caused by the allelic binding of CTCF to the Peg13 DMR. Using an in vitro neuron differentiation system, we show that on the maternal allele, an enhancer-promoter contact formed early in development primes the brain-specific potassium leak channel Kcnk9 for maternal expression prior to neurogenesis. In contrast, this enhancer-promoter contact is blocked by CTCF on the paternal allele, preventing paternal Kcnk9 activation. This work provides a high-resolution map of imprinted chromatin structure and demonstrates that chromatin state established in early development can promote imprinted expression upon differentiation.

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Biallelic non-productive enhancer-promoter interaction precedes imprinted expression of KcnK9 during mouse neural commitment

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

2024-02-05 | GSE244147 | GEO