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Exploring the Stability of Genomic Imprinting and X-Chromosome Inactivation in the Aged Brain (IMPLICON-Seq)

ABSTRACT: Exploring the Stability of Genomic Imprinting and X-Chromosome Inactivation in the Aged Brain (IMPLICON-Seq)

PROVIDER: PRJNA972707 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR24564400_1.fastq.gz	Fastqsanger.gz
	SRR24564400_2.fastq.gz	Fastqsanger.gz
	SRR24564401_1.fastq.gz	Fastqsanger.gz
	SRR24564401_2.fastq.gz	Fastqsanger.gz

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Exploring the Stability of Genomic Imprinting and X-Chromosome Inactivation in the Aged Brain

Project description:Exploring the Stability of Genomic Imprinting and X-Chromosome Inactivation in the Aged Brain

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Exploring the Stability of Genomic Imprinting and X-Chromosome Inactivation in the Aged Brain (RNA-Seq)

Project description:Exploring the Stability of Genomic Imprinting and X-Chromosome Inactivation in the Aged Brain (RNA-Seq)

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Exploring the Stability of Genomic Imprinting and X-Chromosome Inactivation in the Aged Brain (IMPLICON-Seq)

Project description:DNA methylation is a common mechanism regulating monoallelic expression of different genes, including imprinted genes. How age-induced alterations of methylation levels vary across alleles and impact on monoallelic expression is unknown. In the brain, this phenomenon may contribute mechanistically to neuronal dysfunction and disease. In order to investigate the allele-specific transcriptional and epigenetic signatures of aging, we used key brain areas, hippocampus and cerebellum, of juvenile and old hybrid mice obtained from BL6×CAST reciprocal crosses. We set out to explore whether epigenetic drift affects global DNA methylation machinery by investigating 5- methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC) levels. Mass spectrometry analysis showed a significant increase of 5hmC levels in hippocampus of old mice, but this was not accompanied by measurable differences in methylating or demethylating enzymes. The expression of several repetitive elements (LINEs, SINEs, IAP) was also analysed with a reduction of the intracisternal A-particle (IAP) retrotransposons seen in HCP of old mice. We uncovered the allelic-specific DNA methylation profile of aging using genomic imprinting as a read-out by IMPLICON and allelic-expression by RNA sequencing. Here, imprinting is not substantially changed during aging, not affecting their normal monoallelic expression. This work provides the first epigenetic and transcriptional landscape of aging with allelic resolution and confirms that genomic imprinting is a stable epigenetic phenomenon across the whole lifespan.

2024-07-15 | GSE232547 | GEO

Exploring the Stability of Genomic Imprinting and X-Chromosome Inactivation in the Aged Brain (RNA-Seq)

Project description:DNA methylation is a common mechanism regulating monoallelic expression of different genes, including imprinted genes. How age-induced alterations of methylation levels vary across alleles and impact on monoallelic expression is unknown. In the brain, this phenomenon may contribute mechanistically to neuronal dysfunction and disease. In order to investigate the allele specific transcriptional and epigenetic signatures of aging, we used key brain areas, hippocampus and cerebellum, of juvenile and old hybrid mice obtained from BL6×CAST/EiJ (CAST) reciprocal crosses. We set out to explore whether epigenetic drift affects global DNA methylation machinery by investigating 5- methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC) levels. Mass spectrometry analysis showed a significant increase of 5hmC levels in hippocampus of old mice, but this was not accompanied by measurable differences in methylating and demethylating enzymes. The expression of several repetitive elements (LINEs, SINEs, IAP) was also analysed, strictly dependent on 5mC and 5hmC levels, and reporting a reduction of the intracisternal A-particle (IAP) retrotransposons in HCP of old mice. We uncovered the allelic-specific DNA methylation profile of aging using genomic imprinting as a read-out by IMPLICON and allelic expression by RNA sequencing. Here, imprinting is not substantially changed during aging, not affecting their normal monoallelic expression. This work provides the first epigenetic and transcriptional landscape of aging with allelic resolution and confirms that genomic imprinting is a stable epigenetic phenomenon across the whole lifespan.

2024-07-15 | GSE232546 | GEO

Exploring the Stability of Genomic Imprinting and X-Chromosome Inactivation in the Aged Brain

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

2024-07-15 | GSE232548 | GEO

Attrition of X chromosome inactivation in aged hematopoietic stem cells

Project description:During X chromosome inactivation (XCI), the inactive X chromosome (Xi) is recruited to the nuclear lamina at the periphery of the nucleus. Beside X chromosome (X chr) reactivation resulting in a highly penetrant aging-like hematopoietic malignancy, little is known about XCI in aged hematopoietic stem cells (HSCs) . Here, we demonstrate that LaminA/C defines a distinct repressive nuclear compartment for XCI in young HSCs, and its reduction in aged HSCs correlates with an impairment in the overall control of XCI. Integrated omics analyses reveal higher variation in gene expression, global hypomethylation and significantly increased chromatin accessibility on the X chr in aged HSCs. In summary, our data support the role of LaminA/C in the establishment of a special repressive compartment for XCI in HSCs, which is impaired upon aging.

2021-04-07 | GSE167214 | GEO

Attrition of X chromosome inactivation in aged hematopoietic stem cells

Project description:Attrition of X chromosome inactivation in aged hematopoietic stem cells

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Maternal Eed knockout causes loss of H3K27me3 imprinting and random X-inactivation in the extra-embryonic cells

Project description:Genomic imprinting is essential for mammalian development. Recent studies have revealed that maternal histone H3 lysine 27 tri-methylation (H3K27me3) can mediate DNA methylation-independent genomic imprinting. However, the regulatory mechanisms and functions of this new imprinting mechanism are largely unknown. Here we demonstrate that maternal Eed, an essential component of the Polycomb group complex 2 (PRC2), is required for establishing H3K27me3 imprinting. We found that all H3K27me3 imprinted genes, including Xist, lose their imprinted expression in Eed maternal KO (matKO) embryos, resulting in male-biased lethality. Surprisingly, although maternal X chromosome inactivation (XmCI) occurs in Eed matKO embryos at preimplantation due to loss of Xist imprinting, it is resolved at peri-implantation. Ultimately, both X chromosomes are reactivated in the embryonic cell lineage prior to random XCI, and only a single X chromosome undergoes random XCI in the extra-embryonic cell lineage. Thus, our study not only demonstrates an essential role of Eed in H3K27me3 imprinting establishment but also reveals a unique XCI dynamics in the absence of Xist imprinting.

2018-11-26 | GSE116713 | GEO

Xist-mediated Chromosome Inactivation

Project description:Xist-mediated Chromosome Inactivation

| PRJNA489702 | ENA

Genomic imprinting of Xist by maternal H3K27me3

Project description:Maternal imprinting at the Xist gene is essential to achieve paternal allele-specific imprinted X chromosome inactivation (XCI) in female mammals. However, the mechanism underlying the Xist imprinting is unclear. Here we show that the Xist gene is coated with H3K27me3 in mouse oocytes, which persists through preimplantation development. Ectopic removal of H3K27me3 induces maternal Xist expression and maternal XCI, indicating that maternal H3K27me3 is the imprinting mark of Xist.

2017-11-09 | GSE103714 | GEO

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