PRC2-AgeIndex: a universal biomarker of aging and rejuvenation [ChIP-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1067110 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27667471_1.fastq.gz | Fastqsanger.gz | |||
| SRR27667471_2.fastq.gz | Fastqsanger.gz | |||
| SRR27667472_1.fastq.gz | Fastqsanger.gz | |||
| SRR27667472_2.fastq.gz | Fastqsanger.gz | |||
| SRR27667473_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 26 |
Similar Datasets
Project description:PRC2-AgeIndex: a universal biomarker of aging and rejuvenation
| PRJNA1068056 | ENA
Project description:PRC2-AgeIndex: a universal biomarker of aging and rejuvenation [WGBS]
| PRJNA1068062 | ENA
Project description:DNA methylation (DNAm) is one of the most reliable biomarkers of aging across many mammalian tissues. While the age-dependent global loss of DNAm has been well characterized, age-dependent DNAm gain is less specified. Multiple studies have demonstrated that polycomb repressive complex 2 (PRC2) targets are enriched among the CpG sites which gain methylation with age. However, systematic whole-genome examination of all PRC2 targets in the context of aging methylome as well as determination of the pan-tissue or tissue-specific nature of these associations is lacking. Here, by analyzing DNAm data from different assays and from multiple young and old human and mouse tissues, we found that low-methylated regions (LMRs) which are highly bound by PRC2 in embryonic stem cells (PRC2 LMRs) gain methylation with age in all examined somatic mitotic cells. We also estimated that this epigenetic change represents around 90% of the age-dependent DNAm gain genome-wide. Therefore, we propose the “PRC2-AgeIndex,” defined as the average DNAm in PRC2 LMRs, as a universal biomarker of cellular aging in somatic cells. In addition, we demonstrate the application of this biomarker in the evaluation of different anti-aging interventions, including dietary restriction and partial epigenetic reprogramming.
2024-06-19 | GSE253985 | GEO
Project description:DNA methylation (DNAm) is one of the most reliable biomarkers of aging across many mammalian tissues. While the age-dependent global loss of DNAm has been well characterized, age-dependent DNAm gain is less specified. Multiple studies have demonstrated that polycomb repressive complex 2 (PRC2) targets are enriched among the CpG sites which gain methylation with age. However, systematic whole-genome examination of all PRC2 targets in the context of aging methylome as well as determination of the pan-tissue or tissue-specific nature of these associations is lacking. Here, by analyzing DNAm data from different assays and from multiple young and old human and mouse tissues, we found that low-methylated regions (LMRs) which are highly bound by PRC2 in embryonic stem cells (PRC2 LMRs) gain methylation with age in all examined somatic mitotic cells. We also estimated that this epigenetic change represents around 90% of the age-dependent DNAm gain genome-wide. Therefore, we propose the “PRC2-AgeIndex,” defined as the average DNAm in PRC2 LMRs, as a universal biomarker of cellular aging in somatic cells. In addition, we demonstrate the application of this biomarker in the evaluation of different anti-aging interventions, including dietary restriction and partial epigenetic reprogramming.
2024-06-19 | GSE253773 | GEO
Project description:DNA methylation (DNAm) is one of the most reliable biomarkers of aging across mammalian tissues. While the age-dependent global loss of DNAm has been well characterized, DNAm gain is less characterized. Studies have demonstrated that CpGs which gain methylation with age are enriched in Polycomb Repressive Complex 2 (PRC2) targets. However, whole-genome examination of all PRC2 targets as well as determination of the pan-tissue or tissue-specific nature of these associations is lacking. Here, we show that low-methylated regions (LMRs) which are highly bound by PRC2 in embryonic stem cells (PRC2 LMRs) gain methylation with age in all examined somatic mitotic cells. We estimated that this epigenetic change represents around 90% of the age-dependent DNAm gain genome-wide. Therefore, we propose the "PRC2-AgeIndex," defined as the average DNAm in PRC2 LMRs, as a universal biomarker of cellular aging in somatic cells which can distinguish the effect of different anti-aging interventions.
| S-EPMC11250797 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-06-19 | GSE253987 | GEO
Project description:The notion that germline does not age goes back to the 19th century ideas of August Weismann. However, being in a metabolically active state, germline accumulates damage and other age-related changes over time, i.e., they age. For new life to begin in the same young state, they must be rejuvenated in the offspring. Here, we developed a new multi-tissue epigenetic clock and applied it, together with other aging clocks, to track changes in biological age during mouse and human prenatal development. This analysis revealed a significant decrease in biological age, i.e. rejuvenation, during early stages of embryogenesis, followed by an increase in later stages. We further found that pluripotent stem cells do not age even after extensive passaging and that the examined epigenetic age dynamics is conserved across species. Overall, this study uncovers a natural rejuvenation event during embryogenesis and suggests that the minimal biological age (the ground zero) marks the beginning of organismal aging.
2021-05-10 | GSE171332 | GEO
Project description:Aging is associated with a progressive decline in cellular function. To reset the aged cellular phenotype, various reprogramming approaches, including mechanical routes, have been proposed. However, the epigenetic mechanisms underlying cellular rejuvenation are poorly understood. We studied the transcriptional changes in young, aged and mechanically rejuvenated fibroblasts using RNA-seq. The mechanically rejuvenated aged fibroblasts, that had reset their transcription to a younger cell state. In addition, the rejuvenated cells contractile properties were maintained over multiple cell passages. Taken together, our results provide a multi-scale characterization of the chromatin reorganization that accompanies cellular aging and rejuvenation.
2024-03-20 | GSE237269 | GEO
Project description:Aging is a prominent risk factor for neurodegenerative disease, therefore defining mechanisms critical for healthy brain aging should lead to insight into genes that modulate susceptibility to disease. To define such genes, we have pursued analysis of miR-34 mutants in Drosophila. The miR-34 mutant brain displays a gene profile of accelerated aging, and miR-34 upregulation is a potent suppressor of polyglutamine-induced neurodegeneration. We investigated targets of miR-34 to define those important for its functions in mitigating degeneration and impacting health of the brain with age. These studies show that miR-34 targets for silencing two components of polycomb repressive complex 2 (PRC2)—Pcl and Su(z)12—in the brain with age. PRC2 is a histone methyltransferase that confers the repressive H3K27me3 mark, suggesting that a critical role of miR-34 is to modulate the function of PRC2 to silence key genes in the brain with age. Remarkably, gene expression profiling of the brains of hypomorphic mutants in Enhancer of zeste (E(z)), the enzymatic methyltransferase component of PRC2, revealed a younger brain transcriptome profile and identified the small heat shock proteins as key modulated genes. These findings indicate that PRC2 epigenetic mechanisms impact the susceptibility of the brain to degenerative disease with age, and highlight the role of small heat shock proteins to protect the brain from age-associated decline and disease.
2018-10-10 | GSE110135 | GEO
Project description:We combine transient stem cell rejuvenation with targeted removal of senescent cells to test the hypothesis that simultaneously targeting both cell-fate based aging mechanisms will maximize life and health span benefits.
2022-04-24 | GSE201338 | GEO