4,734
Views
142
CrossRef citations to date
0
Altmetric
Point of View

Global heterochromatin loss

A unifying theory of aging?

&
Pages 680-688 | Published online: 01 Jul 2012

Figures & data

Figure 1. Heterochromatin redistribution during aging. Aging is associated with a loss of constitutive heterochromatin, as demonstrated by a decrease in H3K9 methylation and delocalization of HP1 proteins. Concurrently, increases in facultative heterochromatin occur at specific loci, particularly at Senescence-Associated Heterochromatin Foci (SAHFs) that depend on the activity of H3K9 methyltransferases, on recruitment of HP1 proteins and histone chaperones, and on the presence of macro H2A. The decrease in activity of the maintenance DNA methyltransferase Dnmt1 and the increase in de novo Dnmt3 methyltransferases during aging may also contribute to heterochromatin redistribution.

Figure 1. Heterochromatin redistribution during aging. Aging is associated with a loss of constitutive heterochromatin, as demonstrated by a decrease in H3K9 methylation and delocalization of HP1 proteins. Concurrently, increases in facultative heterochromatin occur at specific loci, particularly at Senescence-Associated Heterochromatin Foci (SAHFs) that depend on the activity of H3K9 methyltransferases, on recruitment of HP1 proteins and histone chaperones, and on the presence of macro H2A. The decrease in activity of the maintenance DNA methyltransferase Dnmt1 and the increase in de novo Dnmt3 methyltransferases during aging may also contribute to heterochromatin redistribution.

Figure 2. Epigenetic changes resulting in a decrease and redistribution of global heterochromatin may underlie the various models of aging. The models of free radical accumulation, genetically programmed senescence, telomere shortening, genomic instability, nutritional intake and growth signaling are distinct, yet overlapping theories of aging that may all be linked by heterochromatin redistribution.

Figure 2. Epigenetic changes resulting in a decrease and redistribution of global heterochromatin may underlie the various models of aging. The models of free radical accumulation, genetically programmed senescence, telomere shortening, genomic instability, nutritional intake and growth signaling are distinct, yet overlapping theories of aging that may all be linked by heterochromatin redistribution.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.