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Aging promotes reactivation of the Barr body at distal chromosome regions [RNA Major cardiac cell types]

ABSTRACT: Aging promotes reactivation of the Barr body at distal chromosome regions [RNA Major cardiac cell types]

PROVIDER: PRJNA1147669 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30223449_1.fastq.gz	Fastqsanger.gz
	SRR30223449_2.fastq.gz	Fastqsanger.gz
	SRR30223450_1.fastq.gz	Fastqsanger.gz
	SRR30223450_2.fastq.gz	Fastqsanger.gz
	SRR30223451_1.fastq.gz	Fastqsanger.gz

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Aging promotes reactivation of the Barr body at distal chromosome regions [RNA Major cardiac cell types]

Project description:Decades ago, evidence of age-related reactivation of a single gene on the female inactive X chromosome was observed in mice. While stable silencing of the Barr body is crucial for balancing gene dosage between sexes, it remained unclear whether silencing is maintained during aging. Here, we employed allele-specific multi-omics approaches to capture a comprehensive catalog of genes escaping X chromosome inactivation throughout mouse development and aging. We found substantially elevated escape rates during aging across organs, occurring in multiple distinct cell types and concentrated at distal chromosome regions. Consistently, chromatin accessibility was increased across multiple megabases at chromosome ends, affecting regulatory elements of escapees. Since several age-specific escapees are linked to human diseases, their elevated expression in females might contribute to sex-biased disease progression observed during aging.

2025-03-21 | GSE274690 | GEO

Aging promotes reactivation of the Barr body at distal chromosome regions

Project description:Aging promotes reactivation of the Barr body at distal chromosome regions

| PRJNA1147666 | ENA

Aging promotes reactivation of the Barr body at distal chromosome regions [ATAC]

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Aging promotes reactivation of the Barr body at distal chromosome regions [snRNA]

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Aging promotes reactivation of the Barr body at distal chromosome regions [ATAC]

Project description:Aging promotes reactivation of the Barr body at distal chromosome regions [ATAC]

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Aging promotes reactivation of the Barr body at distal chromosome regions [snRNA]

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Aging promotes reactivation of the Barr body at distal chromosome regions [RNA organs]

Project description:Aging promotes reactivation of the Barr body at distal chromosome regions [RNA organs]

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Aging promotes reactivation of the Barr body at distal chromosome regions

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

2025-03-21 | GSE274695 | GEO

The Histone Demethylase LSD1/ZNF217/CoREST Complex is a Major Restriction Factor of Epstein-Barr Virus Lytic Reactivation

Project description:Epstein-Barr virus (EBV) contributes to ~1.5% of human cancers, including lymphomas, gastric and nasopharyngeal carcinomas. In most of these, nearly 80 viral lytic genes are silenced by incompletely understood epigenetic mechanisms, precluding use of antiviral agents such as ganciclovir to treat the 200,000 EBV-associated cancers/year. To identify host factors critical for EBV latency, we performed a human genome-wide CRISPR-Cas9 screen in Burkitt B-cells. Top hits included the lysine-specific histone demethylase LSD1 and its co-repressors ZNF217 and CoREST. LSD1 removes histone 3 lysine 4 (H3K4) and histone 3 lysine 9 (H3K9) methylation marks to downmodulate chromatin activation. LSD1, ZNF217 or CoREST knockout triggered EBV reactivation, as did a LSD1 small molecule antagonist, whose effects were additive with histone deacetylase inhibition. LSD1 blockade reactivated EBV in Burkitt lymphoma, gastric carcinoma and nasopharyngeal carcinoma models, sensitized cells to ganciclovir cytotoxicity and induced EBV reactivation in murine xenografts. ZNF217 and LSD1 co-occupied the EBV immediate early gene BZLF1 promoter, which drives B-cell lytic cycle, as well as to the oriLyt enhancer regions recently implicated in EBV reactivation. LSD1 depletion increased levels of activating histone 3 lysine 4 (H3K4) methylation but not repressive histone lysine 9 methylation marks at BZLF1 and oriLyt and induced their interaction by long-range DNA looping. An orthogonal CRISPR screen highlighted a key H3K4 methyltransferase KMT2D role in driving EBV reactivation. Our results highlight H3K4 methylation as a major EBV lytic switch regulator and suggest novel therapeutic approaches.

2025-02-19 | GSE284859 | GEO

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