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Status |
Public on Mar 17, 2023 |
Title |
A hyper-quiescent chromatin state formed during aging is reversed by regeneration |
Organism |
Mus musculus |
Experiment type |
Methylation profiling by high throughput sequencing
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Summary |
Epigenetic alterations are a key hallmark of aging but have not been extensively explored in tissues. Here, using naturally aged murine liver as a model and extending study to other quiescent tissues, we find that aging is driven by temporal chromatin alterations that promote a refractory cellular state and compromise cellular identity. Using an integrated multi-omics approach and the first direct visualization of aged chromatin, we find that old cells show global H3K27me3-driven broad heterochromatinization and transcription suppression. At the local level, site-specific loss of H3K27me3 from promoters of genes encoding developmental transcription factors leads to expression in liver of non-hepatocyte markers. Interestingly, liver regeneration reverses H3K27me3 patterns and rejuvenates multiple molecular and physiological aspects of the aged liver.
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Overall design |
meDIP-seq in 4 young (12-18 weeks) and 4 old (81-90 weeks) mouse livers
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Contributor(s) |
Yang N, Sen P |
Citation missing |
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Submission date |
Jan 23, 2023 |
Last update date |
Mar 19, 2023 |
Contact name |
Supriyo De |
Organization name |
NIA-IRP, NIH
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Department |
Laboratory of Genetics and Genomics
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Lab |
Computational Biology & Genomics Core
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Street address |
251 Bayview Blvd
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City |
Baltimore |
State/province |
Maryland |
ZIP/Postal code |
21224 |
Country |
USA |
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Platforms (1) |
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Samples (16)
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This SubSeries is part of SuperSeries: |
GSE185708 |
A hyper-quiescent chromatin state is a barrier to productive regeneration during aging. |
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Relations |
BioProject |
PRJNA926514 |