p53 and p16INK4A independent induction of senescence by chromatin-dependent alteration of S-phase progression
Open accessAbstract
Senescence is triggered by various cellular stresses that result in genomic lesions and DNA damage response activation. However, the role of chromatin and DNA replication in senescence induction remains elusive. Here we show that downregulation of p300 histone acetyltransferase activity induces senescence by a mechanism that is independent of the activation of p53, p21(CIP1) and p16(INK4A). This inhibition leads to a global H3, H4 hypoacetylation, initiating senescence-associated heterochromatic foci formation during S phase, together with a global decrease in replication fork velocity, and alteration of DNA replication timing. This replicative stress occurs without DNA damage and checkpoint activation, but results in a robust G2/M cell cycle arrest, within only one cell cycle. These results provide new insights into the control of S-phase progression by p300, and identify an unexpected chromatin-dependent alternative mechanism for senescence induction, which could possibly be exploited to treat cancer by senescence induction without generating further DNA damage.
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p300 knockdown causes H3/H4 hypoacetylation and increased senescence in human cells, providing evidence for a causative chromatin-senescence link.
“knockdown of the histone acetyltransferase p300 results in hypoacetylation of histones H3 and H4 and an increase in senescence in human cells, providing evidence for a causative link between changes in chromatin state and senescence (Prieur et al., 2011).”
From The Aging Epigenome (2016) · cites this paper as Prieur et al., 2011
This chromatin-based senescence induction occurred independently of DNA damage and CDK inhibition pathway (p53/p21/p16).
“this chromatin-based induction of senescence occurred independently of other mechanisms of inducing senescence, including DNA damage and activation of the CDK inhibition pathway (p53/p21/p16) (Prieur et al., 2011).”
From The Aging Epigenome (2016) · cites this paper as Prieur et al., 2011
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- Authors
- Prieur, A., Besnard, E., Babled, A., & Lemaitre, J.-M.
- Affiliations
- Inserm (FR)
- ORCID
- Prieur, Alexandre
- Venue
- Nature Communications
- Published
- 2011-09-13
- Volume
- 2
- Issue
- 1
- Pages
- 473-473
- ISSN
- 2041-1723 (ISSN-L)
- OpenAlex
- W2075178830
- Cited by
- 117
- References
- 48
- Citations by year
- 2026: 11 · 2025: 9 · 2024: 9 · 2023: 7 · 2022: 5 · 2021: 9 · 2020: 6 · 2019: 14 · 2018: 10 · 2017: 4 · 2016: 8 · 2015: 9 · 2014: 4 · 2013: 6 · 2012: 6
- FWCI
- 3.49
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Institut National de la Santé et de la Recherche Médicale
- Fondation pour la Recherche Médicale
- Institut National Du Cancer
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- cellular senescence, P300, histone acetyltransferase, histone hypoacetylation, S phase progression, DNA replication timing, replicative stress, senescence-associated heterochromatin foci, G2/M cell cycle arrest, p53-independent senescence, p21, chromatin
- MeSH terms
- Acetylation, Cell Line, Chromatin, DNA Damage, DNA Replication, Flow Cytometry, Humans, Tumor Suppressor Protein p53, S Phase, Cellular Senescence, Cyclin-Dependent Kinase Inhibitor p16
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