DNA damage, chromatin, and transcription: the trinity of aging
Open accessAbstract
Aging brings about numerous cellular defects. Amongst the most prominent are elevated levels of persistent DNA damage, changes to chromatin structure and epigenetic modifications, and alterations of global transcription programs. These are not independent events and recent work begins to shed light on the intricate interplay between these aging-related defects.
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Accumulation of DNA damage during life could be a source of age-associated epigenomic changes, and chromatin state could affect DNA repair.
“Interestingly, sensing and responding to DNA damage involves the recruitment of chromatin modifiers, suggesting that an accumulation of DNA damage during life could be a source for age-associated epigenomic changes and that changes in chromatin state could affect DNA repair (Burgess et al., 2012; Oberdoerffer and Sinclair, 2007).”
From The Aging Epigenome (2016) · cites this paper as Burgess et al., 2012
A compact chromatin domain that enhances DDR signaling complements the need for chromatin relaxation to amplify and activate DDR effector pathways.
“The establishment of a compact chromatin domain for enhancing DDR signaling is complementary to the observation that chromatin relaxation is required for amplification and activation of DDR effector pathways, and they likely occur in a dynamic exchange (Burgess et al., 2012; Soria et al., 2012).”
From Activation of DNA Damage Response Signaling by Condensed Chromatin (2014) · cites this paper as Burgess et al., 2012
Chromatin compaction and relaxation probably occur in a dynamic exchange.
“The establishment of a compact chromatin domain for enhancing DDR signaling is complementary to the observation that chromatin relaxation is required for amplification and activation of DDR effector pathways, and they likely occur in a dynamic exchange (Burgess et al., 2012; Soria et al., 2012).”
From Activation of DNA Damage Response Signaling by Condensed Chromatin (2014) · cites this paper as Burgess et al., 2012
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References 62 · Cited by 72
- Authors
- Burgess, R. C., Misteli, T., & Oberdoerffer, P.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Misteli, Tom
- Venue
- Current Opinion in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2012-12
- Volume
- 24
- Issue
- 6
- Pages
- 724-730
- ISSN
- 0955-0674 (ISSN-L)
- PMC
- PMC3524355
- OpenAlex
- W2019741013
- Cited by
- 72
- References
- 62
- Citations by year
- 2026: 3 · 2025: 1 · 2023: 1 · 2022: 3 · 2021: 21 · 2020: 6 · 2019: 2 · 2018: 3 · 2017: 4 · 2016: 6 · 2015: 6 · 2014: 7 · 2013: 9
- FWCI
- 0.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (ZIABC010309)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- aging, DNA damage, chromatin structure, epigenetic modifications, transcription, cellular senescence, epigenetic aging, transcriptional programs
- MeSH terms
- Aging, Animals, Chromatin, DNA Damage, DNA Repair, Humans, RNA Processing, Post-Transcriptional, Transcription, Genetic, Signal Transduction
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