The heterochromatin loss model of aging

@article{Villeponteau1997TheHL,
  title={The heterochromatin loss model of aging},
  author={B. Villeponteau},
  journal={Experimental Gerontology},
  year={1997},
  volume={32},
  pages={383-394}
}
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… Expand

Paper Mentions

Interventional Clinical Trial
This open-label field trial evaluates the effects of treatment with a multi-pathway dietary supplement (Stem Cell 100+) that has been commercially available for several years. The… Expand
ConditionsBlood Pressure, Concentration Ability Impaired, Energy Supply; Deficiency, (+6 more)
InterventionDietary Supplement
Heterochromatin Formation Promotes Longevity and Represses Ribosomal RNA Synthesis
TLDR
Results suggest that epigenetic preservation of genome stability, especially at the rDNA locus, and repression of unnecessary rRNA synthesis, might be an evolutionarily conserved mechanism for prolonging lifespan. Expand
Chromatin structure and transposable elements in organismal aging
TLDR
This review summarizes the recent evidence linking chromatin structure and function to aging, with a particular focus on the relationship of heterochromatin structure to organismal aging. Expand
H3K27 modifiers regulate lifespan in C. elegans in a context-dependent manner
TLDR
Overall, this work suggests that the heterochromatin loss model of ageing may be too simplistic an explanation of organismal ageing when molecular and tissue-specific effects are taken into account. Expand
Roles of Topoisomerases in Heterochromatin, Aging, and Diseases
TLDR
It is proposed that topological stress may be generated in both DNA and RNA during heterochromatin formation and function, which depend on multiple topoisomerases to resolve. Expand
Global heterochromatin loss
TLDR
The objective of this Point-of-View is to highlight recent progress on the “loss of heterochromatin” model of aging and to propose that epigenetic changes contributing to global heterochrome loss may underlie the various cellular processes associated with aging. Expand
The role of transposable elements activity in aging and their possible involvement in laminopathic diseases
TLDR
The possible role of the nuclear lamina, a major player in heterochromatin dynamics, in the regulation of transposable element activity and potential implications in laminopathic diseases is discussed. Expand
The Epigenome of Aging
TLDR
The role of epigenetic modulators in DNA damage response pathway as well as heterochromatin formation and the alterations effected by these modulators on the epigenome during aging are focused on. Expand
Sir2 links chromatin silencing, metabolism, and aging.
TLDR
A speculative model of how a gradual disruption in chromatin silencing may occur and how such a change may cause aging is presented, which is widely observed in many organisms. Expand
Erratum to: Analysis of gene expression during aging of CGNs in culture: implication of SLIT2 and NPY in senescence
TLDR
The results showed that the two genes neuropeptide Y (Npy) and Slit homolog 2 (Drosophila) (Slit2) gradually increase during aging, and upon suppression of these two genes, there was gradual increase in cell viability along with restoration of the expression of Topo IIβ and potential repair proteins. Expand
The great unravelling: chromatin as a modulator of the aging process.
TLDR
This review explores the current state of the understanding of the links between chromatin organization and aging and investigates changes in chromatin states that have emerged as potentially central conduits of mammalian aging. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 73 REFERENCES
Heterochromatin and gene expression in Drosophila.
TLDR
The models and experimental data that address the mechanisms of PEV in different cell types, the potential functions of modifiers ofPEV, and the relationship of PEv to other phenomena associated with variegated gene expression in Drosophila are evaluated. Expand
Position effect variegation and chromatin proteins
  • Gunter Reute, P. Spierer
  • Biology, Medicine
  • BioEssays : news and reviews in molecular, cellular and developmental biology
  • 1992
TLDR
PEV has been intensively investigated in the fruitfly Drosophila, where the phenomenon allows a genetic dissection of chromatin components and demonstrates that genetic, molecular and developmental analysis of these genes provides an avenue to the identification of regulatory and structural chromatin Components and hence to fundamental aspects of chromosome structure and function. Expand
Effect of replicative age on transcriptional silencing near telomeres in Saccharomyces cerevisiae.
TLDR
Changes in silencing in the URA3 gene raise the possibility that the transcriptional status of genes in the subtelomeric region may be important for the senescence of both dividing cells and postmitotic cells, in which telomeres remain constant in length. Expand
Mutation in the silencing gene S/R4 can delay aging in S. cerevisiae
TLDR
It is suggested that sir4-42 extends life span by preventing recruitment of the SIR proteins to HM loci and telomeres, thereby increasing their concentration at other chromosomal regions, and maintaining silencing at these other regions may be critical in preventing aging. Expand
Loss of Transcriptional Silencing Causes Sterility in Old Mother Cells of S. cerevisiae
TLDR
These findings pinpoint the molecular cause of an aging-specific phenotype in yeast and provide direct evidence for a breakdown of silencing in old cells, as predicted from earlier findings that SIR4 is a determinant of life span in this organism. Expand
Replicative senescence: Considerations relating to the stability of heterochromatin domains
  • B. Howard
  • Medicine, Biology
  • Experimental Gerontology
  • 1996
TLDR
The possibility is considered that defects in cell cycle-coupled reassembly of repressive chromatin domains may contribute to HDF senescence, a model based on telomere shortening and loss of DNA methylation. Expand
Cell lineage‐specific expression of modulo, a dose‐dependent modifier of variegation in Drosophila.
TLDR
Based on its dominant phenotype, expression pattern and DNA‐binding activity of its product, it is proposed that mod regulates chromatin structure and activity in specific cell lineages. Expand
A sequence motif found in a Drosophila heterochromatin protein is conserved in animals and plants.
Modifiers of position-effect-variegation in Drosophila encode proteins that are thought to modify chromatin, rendering it heritably changed in its expressibility. In an attempt to identify similarExpand
The SIR2 gene family, conserved from bacteria to humans, functions in silencing, cell cycle progression, and chromosome stability.
TLDR
The discovery of four Saccharomyces cerevisiae homologs of the SIR2 silencing gene (HSTs), as well as conservation of this gene family from bacteria to mammals are reported, establishing new connections between silencing and these fundamental cellular processes. Expand
Chromatin reorganization during senescence of proliferating cells.
TLDR
The remodeling occurring in the cell through serial divisions seems to take place in such a way as to decrease the probability of further reorganizations, tending to a limit, and the decline of the proliferative activity seems to be the result of the tendency to reach this limit. Expand
...
1
2
3
4
5
...