Abstract
Chromatin 3D structure is highly dynamic and associated with many biological processes, such as cell cycle progression, cellular differentiation, cell fate reprogramming, cancer development, cellular senescence, and aging. Recently, by using chromosome conformation capture technologies, tremendous findings have been reported about the dynamics of genome architecture, their associated proteins, and the underlying mechanisms involved in regulating chromatin spatial organization and gene expression. Cellular senescence and aging, which involve multiple cellular and molecular functional declines, also undergo significant chromatin structural changes, including alternations of heterochromatin and disruption of higher-order chromatin structure. In this review, we summarize recent findings related to genome architecture, factors regulating chromatin spatial organization, and how they change during cellular senescence and aging.
Highlights
Aging is a complex biological process that involves multiple cellular and molecular functional declines, including cellular senescence, genomic instability, and epigenetic alterations [1]
Global loss of heterochromatic regions and reduction of repressive histone modification markers occur in many aged eukaryotic species and senescent cell types, a gain of heterochromatin is found in oncogene-induced senescent (OIS) cells that form senescence-associated heterochromatin foci (SAHF) [6]
Shimi et al reported that, in WI-38 fibroblasts, knockdown of lamin B1 slows cell growth and triggers premature senescence, while overexpression of lamin B1 promotes proliferation and delays the onset of senescence [126]. These results reveal the essential roles of lamin proteins in chromatin structures, chromosome territories, and longevity
Summary
Aging is a complex biological process that involves multiple cellular and molecular functional declines, including cellular senescence, genomic instability, and epigenetic alterations [1]. Significant chromatin structural changes occur during physiological aging and senescence, from alterations in the nuclear envelope and the structure of chromosome territories within the nucleus to changes in nucleosome positioning and histone modifications [2,3,4]. These chromatin changes include global histone loss, the alternation of epigenetic landscapes, chromatin spatial interaction changes, loss of heterochromatic regions, and large-scale chromatin rearrangements. Follow-up studies with higher data resolution revealed that individual chromosomes are partitioned into topologically associating domains (TADs), which are highly conserved across cell types and species. We discuss recent findings regarding chromatin organization, the factors that regulate it, and how they change during physiological aging, premature aging syndromes, and cellular senescence
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