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- W2966379217 abstract "Summary S-adenosylmethionine (SAM) is the methyl-donor substrate for DNA and histone methyltransferases that regulate cellular epigenetic states. This metabolism-epigenome link enables the sensitization of chromatin methylation to altered SAM abundance. However, a chromatin-wide understanding of the adaptive/responsive mechanisms that allow cells to actively protect epigenetic information during life-experienced fluctuations in SAM availability are unknown. We identified a robust response to SAM depletion that is highlighted by preferential cytoplasmic and nuclear de novo mono-methylation of H3 Lys 9 (H3K9) at the expense of global losses in histone di- and tri-methylation. Under SAM-depleted conditions, de novo H3K9 mono-methylation preserves heterochromatin stability and supports global epigenetic persistence upon metabolic recovery. This unique chromatin response was robust across the mouse lifespan and correlated with improved metabolic health, supporting a significant role for epigenetic adaptation to SAM depletion in vivo . Together, these studies provide the first evidence for active epigenetic adaptation and persistence to metabolic stress." @default.
- W2966379217 created "2019-08-13" @default.
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- W2966379217 date "2019-08-06" @default.
- W2966379217 modified "2023-09-27" @default.
- W2966379217 title "Methyl-Metabolite Depletion Elicits Adaptive Responses to Support Heterochromatin Stability and Epigenetic Persistence" @default.
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- W2966379217 doi "https://doi.org/10.1101/726448" @default.
- W2966379217 hasPublicationYear "2019" @default.
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