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The heterochromatin loss model of aging

Villeponteau, Bryant·1997·Experimental Gerontology

Abstract

There are significant changes in gene expression that occur with cellular senescence and organismic aging. Genes residing in compacted heterochromatin domains are typically silenced due to an altered accessibility to transcription factors. Heterochromatin domains and gene silencing are set up in early development and were initially believed to be maintained for the remainder of the lifespan. Recent data suggest that there may be a net loss of heterochromatin with advancing age in both yeast and mice. The gradual loss of heterochromatin-induced gene silencing could explain the changes in gene expression that are closely linked with aging. A general model is proposed for heterochromatin loss as a major factor in generating alterations in gene expression with age. The heterochromatin loss model is supported by several lines of evidence and suggests that a fundamental genetic mechanism underlies most of the changes in gene expression observed with senescence.

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Crossref · 10.1016/s0531-5565(96)00155-6

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  • Epigenetic networks are delicate and their disruption probably initiates other events that cause cells to lose their function over time.

    “suggesting that epigenetic networks are delicate and that their disruption probably initiates other events that cause cells to lose their function over time 8,9 .”
  • Perturbing epigenetic networks leads to extensive changes in gene expression that directly impact proteostasis, nutrient sensing, senescence and several other hallmarks of aging.

    “Perturbing these epigenetic networks leads to extensive changes in gene expression that directly impact proteostasis, nutrient sensing, senescence and several other hallmarks of aging, suggesting that epigenetic networks are delicate and that their disruption probably initiates other events that cause cells to lose their function over time 8,9 .”

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Metadata

Authors
Villeponteau, B.
Venue
Experimental Gerontology
Publisher
Elsevier BV
Published
1997-07
Volume
32
Issue
4-5
Pages
383-394
ISSN
0531-5565
Cited by
237
References
8
Language
en

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