Genomes of replicatively senescent cells undergo global epigenetic changes leading to gene silencing and activation of transposable elements
Open accessAbstract
Summary: Replicative cellular senescence is an important tumor suppression mechanism and also contributes to aging. Progression of both cancer and aging include significant epigenetic components, but the chromatin changes that take place during cellular senescence are not known. We used formaldehyde assisted isolation of regulatory elements ( FAIRE ) to map genome‐wide chromatin conformations. In contrast to growing cells, whose genomes are rich with features of both open and closed chromatin, FAIRE profiles of senescent cells are significantly smoothened. This is due to FAIRE signal loss in promoters and enhancers of active genes, and FAIRE signal gain in heterochromatic gene‐poor regions. Chromatin of major retrotransposon classes, Alu, SVA and L1, becomes relatively more open in senescent cells, affecting most strongly the evolutionarily recent elements, and leads to an increase in their transcription and ultimately transposition. Constitutive heterochromatin in centromeric and peri‐centromeric regions also becomes relatively more open, and the transcription of satellite sequences increases. The peripheral heterochromatic compartment ( PHC ) becomes less prominent, and centromere structure becomes notably enlarged. These epigenetic changes progress slowly after the onset of senescence, with some, such as mobilization of retrotransposable elements becoming prominent only at late times. Many of these changes have also been noted in cancer cells.
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Oncogene-induced senescent cells and late replicatively senescent fibroblasts show increased nucleosomal chromatin accessibility, with most open regions mapping to regulatory elements and repeats.
“oncogene-induced senescent cells and late replicatively senescent fibroblasts exhibit a marked increase in chromatin accessibility at the nucleosomal level, with most of the open chromatin regions mapping to regulatory elements and repeats66,67”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [67]
The Discussion (page unavailable) describes relatively more open chromatin at repeats and other gene-poor regions in replicatively senescent cells, with changes most evident after prolonged senescence. It also describes reduced accessibility at active regulatory regions. This paper does not establish the claim for oncogene-induced senescence or show that most open regions map to regulatory elements and repeats. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSenescent cells exhibit a global increase in chromatin accessibility, but the genome-wide profile varies depending on the stimulus.
“Senescent cells also exhibit a global increase in chromatin accessibility, but the genome-wide profile varies depending on the stimulus (De Cecco et al., 2013).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as De Cecco et al., 2013
The Abstract and Discussion report genome-wide changes in chromatin accessibility during replicative senescence, including opening in gene-poor regions. They also report closing in gene-rich regions, so they do not establish a global increase in accessibility. The cited passages do not compare senescence-inducing stimuli or show that the genome-wide profile varies by stimulus. (LLM, conf=0.83)
Experimental — accuracy not yet measuredNormally repressed LINE-1 retrotransposons are activated in senescence, stimulating the cGAS-STING pathway that elicits a type 1 interferon response.
“The normally repressed LINE-1 (L1) retrotransposons are activated, stimulating the cGAS-STING pathway that elicits a type 1 interferon response (see Secretion) (De Cecco et al., 2013).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as De Cecco et al., 2013
The Results (page unavailable) report that L1 RNA expression increased in senescent cells, and the Discussion describes retrotransposons as normally repressed. The paper does not address cGAS-STING stimulation or a type I interferon response, so it supports only the L1-activation part of the sentence. (LLM, conf=0.91)
Experimental — accuracy not yet measuredRetrotransposons become reactivated in cell senescence and with age in both mammals and Drosophila.
“Retrotransposons become reactivated in cell senescence and with age in both mammals and Drosophila58, 60, 66, 68.”
From The role of retrotransposable elements in ageing and age-associated diseases (2021) · cites this paper as [66]
The Results (page unavailable in our copy) report increased Alu and L1 RNA expression in senescent human cells. The Discussion also notes L1 activation in aging brain tissue, but our copy does not report retrotransposon reactivation with age or senescence in Drosophila; a search for Drosophila found no such passage. (LLM, conf=0.88)
Experimental — accuracy not yet measuredLoss of lamin-associated domains has been primarily investigated via electron microscopy techniques.
“The ability of STORM to provide a detailed rendering of the structure of chromatin fibers37 makes it ideal to investigate changes in heterochromatin distribution within senescent nuclei, such as the loss of lamin-associated domains38, which has been primarily investigated via electron microscopy techniques39.”
From Spatial mapping of cellular senescence: emerging challenges and opportunities (2023) · cites this paper as [39]
The Results (page not provided) report using electron microscopy to find reduced staining of peripheral heterochromatin in senescent nuclei. The paper does not establish that lamin-associated domains themselves were lost or that their loss has primarily been investigated by electron microscopy. (LLM, conf=0.84)
Experimental — accuracy not yet measured
A conserved feature of aging is the progressive increase in retrotransposon transcript levels, particularly the ERV class of LTR retrotransposons.
“A conserved feature of aging is the progressive increase in retrotransposon transcript levels, particularly the ERV class of LTR retrotransposons”
From The Role of Retrotransposons and Endogenous Retroviruses in Age-Dependent Neurodegenerative Disorders (2024) · cites this paper as De Cecco et al. 2013
The Results (page not provided) report increased Alu and L1 RNA in senescent cells, and the Discussion says retrotransposon expression changes emerge after cells have remained senescent for weeks. The paper studies replicative senescence, not a conserved increase across aging, and the cited passages do not establish a particular increase in ERV-class LTR retrotransposons. (LLM, conf=0.87)
Experimental — accuracy not yet measuredL1s become more transcriptionally active during aging and senescence.
“this study builds on the mounting body of evidence which suggests that L1s become more transcriptionally active during aging and senescence10,49”
From SIRT6 represses LINE1 retrotransposons by ribosylating KAP1 but this repression fails with stress and age (2014) · cites this paper as [10]
The Results report increased L1 RNA expression in replicatively senescent cells (Fig. 3C), supporting the senescence portion of the claim. The Discussion links aging to changes that could permit transposable-element expression, but does not report increased L1 transcription during organismal aging. (LLM, conf=0.86)
Experimental — accuracy not yet measuredDecompacted hSATII loci are a characteristic feature of senescent fibroblasts.
“These findings suggest that decompacted hSATII loci are a characteristic feature of senescent fibroblasts, consistent with previous reports on satellite distension during senescence (23–25).”
From Chromatin conformational changes at human satellite II contribute to the senescence phenotype in the tumor microenvironment (2023) · cites this paper as [23]
Chromatin loosening at genomic repeats increases expression of transposable elements, which are normally epigenetically silenced and dormant in unstressed cells.
“Chromatin loosening at genomic repeats results in increased expression levels of transposable elements, which are normally epigenetically silenced and dormant in unstressed cells67”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [67]
Senescence-associated distension of satellites corresponds to de-compaction of (peri-)centric constitutive heterochromatin.
“Another chromatin feature, termed senescence-associated distension of satellites (SADSs), corresponds to de-compaction of (peri-)centric constitutive heterochromatin (Cruickshanks et al., 2013; De Cecco et al., 2013; Swanson et al., 2013).”
From Cellular Senescence: Defining a Path Forward (2019) · cites this paper as De Cecco et al., 2013
Increased chromatin accessibility of pericentromeric hSATII loci in senescent fibroblasts as determined by FAIRE-seq and ATAC-seq validated this distention.
“Increased chromatin accessibility of the pericentromeric hSATII loci in senescent fibroblasts as determined by formaldehyde-assisted isolation of regulatory element sequencing (23) and assay for transposase-accessible chromatin with sequencing (ATAC-seq) validated this distention (11, 21).”
From Chromatin conformational changes at human satellite II contribute to the senescence phenotype in the tumor microenvironment (2023) · cites this paper as [23]
hSATII transcription is elevated in senescent and tumor cells.
“hSATII transcription is elevated in senescent (11, 23, 25, 26) and tumor cells (27–32)”
From Chromatin conformational changes at human satellite II contribute to the senescence phenotype in the tumor microenvironment (2023) · cites this paper as [23]
hSATII DNA adopts a dramatically open conformation in senescent human diploid fibroblasts as determined by DNA-FISH.
“Although the hSATII DNA is generally silenced by heterochromatinization, it adopts a dramatically open conformation in senescent human diploid fibroblasts as determined by DNA-fluorescence in situ hybridization (DNA-FISH) (23).”
From Chromatin conformational changes at human satellite II contribute to the senescence phenotype in the tumor microenvironment (2023) · cites this paper as [23]
Decondensation of these heterochromatic regions is associated with expression of transposable elements (such as LINE1) and their transposition, particularly at later time points after senescence induction.
“The decondensation of these heterochromatic regions is associated with expression of transposable elements (such as LINE1 elements) and their transposition, particularly at later time points after the induction of senescence.”
From Cellular senescence and its effector programs (2014) · cites this paper as De Cecco et al. 2013
Chromatin of repetitive sequences, including major classes of retrotransposon and pericentromeric regions, tends to become open in senescent cells.
“On the other hand, chromatin of repetitive sequences, including major classes of retrotransposon as well as pericentromeric regions, which are highly condensed in normal cells, tend to become open in senescent cells.”
From Cellular senescence and its effector programs (2014) · cites this paper as De Cecco et al. 2013
In replicative senescent HDFs, there is an overall condensation of chromatin in euchromatic regions, with the exception of some specific genes.
“They showed, in replicative senescent HDFs, an overall condensation of chromatin in euchromatic regions, with the exception of some specific genes.”
From Cellular senescence and its effector programs (2014) · cites this paper as De Cecco et al. 2013
Mechanisms that silence retrotransposons in somatic cells are not completely efficient and may deteriorate with age.
“evidence has begun to accumulate indicating that the mechanisms which silence retrotransposons in somatic cells are not completely efficient9 and may deteriorate with age10,11.”
From SIRT6 represses LINE1 retrotransposons by ribosylating KAP1 but this repression fails with stress and age (2014) · cites this paper as [10]
Primer sequences were analyzed with an in silico PCR tool to determine how many genomic elements contribute to each amplification product.
“Primer sequences were analyzed using the UCSC genome browser in silico PCR tool (genome.ucsc.edu/cgi-bin/hgPcr) to determine the number of genomic elements that contribute to the amplification products (De Cecco et al., 2013).”
From Loss of epigenetic information as a cause of mammalian aging (2023) · cites this paper as De Cecco et al., 2013
The Experimental procedures section on PCR primer design refers readers to supplemental methods, while the Results say that some primers were empirically verified to amplify individual elements with single-copy kinetics. Neither passage says primer sequences were analyzed with the UCSC in silico PCR tool to count the genomic elements contributing to amplification products; searches for that tool and purpose found no such passage in our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measuredTransposons can be produced in senescent cells, re-insert into their DNA, contribute to the senescent phenotype, and exacerbate the SASP.
“Transposons (“jumping genes”) can be produced within senescent cells that re-insert into senescent cell DNA, contributing to the senescent cell phenotype and exacerbating their SASP [24, 25].”
From Reducing Senescent Cell Burden in Aging and Disease (2020) · cites this paper as [24]
In late-passage human cell culture, senescent cells have more open chromatin at Alu, L1, and SVA elements.
“the chromatin at transposable elements (Alu, L1, and SVA) becomes more open (De Cecco et al., 2013).”
From The Aging Epigenome (2016) · cites this paper as De Cecco et al., 2013
Expression of repetitive DNA elements increases in senescent cells.
“the expression of these repetitive DNA elements also increases in senescent cells (De Cecco et al., 2013).”
From The Aging Epigenome (2016) · cites this paper as De Cecco et al., 2013
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- Authors
- De Cecco, M., Criscione, S. W., Peckham, E. J., Hillenmeyer, S., Hamm, E. A., Manivannan, J., Peterson, A. L., Kreiling, J. A., Neretti, N., & Sedivy, J. M.
- Affiliations
- Department of Molecular Biology, Cell Biology and Biochemistry, Center for Genomics and Proteomics Brown University Providence 02912 RI USA
- Brown University (US)
- Corresponding author
- Neretti, Nicola
- Sedivy, John M.
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2013-01-30
- Volume
- 12
- Issue
- 2
- Pages
- 247-256
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC3618682
- OpenAlex
- W2065557328
- Cited by
- 459
- References
- 51
- Citations by year
- 2026: 21 · 2025: 41 · 2024: 51 · 2023: 34 · 2022: 38 · 2021: 42 · 2020: 43 · 2019: 33 · 2018: 34 · 2017: 30 · 2016: 29 · 2015: 25 · 2014: 24 · 2013: 12
- FWCI
- 20.83
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Aging Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (K25AG028753, R37AG016694, K01AG039410)
- National Institute of General Medical Sciences (P30GM103410, P30 GM0103410, T32GM007601)
- National Center for Research Resources (P20RR015578)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- epigenetic modifications, chromatin conformation, FAIRE, transposable elements, Alu elements, SVA elements, heterochromatin, centromere, satellite DNA, gene silencing, tumor suppression, aging
- MeSH terms
- Cells, Cultured, Centromere, DNA Transposable Elements, Fibroblasts, Formaldehyde, Heterochromatin, Humans, Transcription, Genetic, Gene Expression, Genome, Human, Cellular Senescence, Oligonucleotide Array Sequence Analysis, Gene Silencing, Euchromatin, Epigenesis, Genetic, Regulatory Elements, Transcriptional
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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