A genomics approach identifies senescence‐specific gene expression regulation
Open accessAbstract
Summary: Replicative senescence is a fundamental tumor‐suppressive mechanism triggered by telomere erosion that results in a permanent cell cycle arrest. To understand the impact of telomere shortening on gene expression, we analyzed the transcriptome of diploid human fibroblasts as they progressed toward and entered into senescence. We distinguished novel transcription regulation due to replicative senescence by comparing senescence‐specific expression profiles to profiles from cells arrested by DNA damage or serum starvation. Only a small specific subset of genes was identified that was truly senescence‐regulated and changes in gene expression were exacerbated from presenescent to senescent cells. The majority of gene expression regulation in replicative senescence was shown to occur due to telomere shortening, as exogenous telomerase activity reverted most of these changes.
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A group of genes encoding proteins involved in spindle assembly and chromosome segregation, such as CENP-E, are downregulated in senescent cells.
“Moreover, a group of genes encoding proteins involved in spindle assembly and chromosome segregation, such as CENP-E, are downregulated [137,140].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [140]
DNA repair and chromatin organization genes are downregulated in senescent cells.
“DNA repair and chromatin organization genes are downregulated [133,139,140].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [140]
Genes involved in membrane trafficking and intercellular signaling, such as cell-cell adhesion molecules and cell-surface receptors, are upregulated in senescent cells.
“Conversely, genes involved in membrane trafficking and intercellular signaling, such as cell–cell adhesion molecules and cell–surface receptors, are upregulated in senescent cells [133,140].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [140]
Genes encoding factors that promote cell cycle arrest, such as CDK inhibitors, are upregulated upon senescence induction.
“Genes encoding factors that promote cell cycle arrest, such as CDK inhibitors, are upregulated upon senescence induction [139,140].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [140]
In senescence-associated transcriptome signatures, genes involved in growth factor signaling, cell cycle progression, DNA replication, and mitosis progression control are downregulated.
“In these senescence-associated signatures, genes involved in growth factor signaling, cell cycle progression, DNA replication, and mitosis progression control are downregulated [68,136,137,138,139,140].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [140]
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- Authors
- Lackner, D. H., Hayashi, M. T., Cesare, A. J., & Karlseder, J.
- Affiliations
- Salk Institute for Biological Studies (US)
- Corresponding author
- Karlseder, Jan
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2014-05-23
- Volume
- 13
- Issue
- 5
- Pages
- 946-950
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC4172521
- OpenAlex
- W1964295923
- Cited by
- 47
- References
- 19
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2023: 4 · 2022: 2 · 2021: 4 · 2020: 4 · 2019: 5 · 2018: 4 · 2017: 5 · 2016: 5 · 2015: 4 · 2014: 5
- FWCI
- 4.21
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Aging Cell (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (GM087476, CA174942)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- replicative senescence, telomere shortening, gene expression regulation, transcriptome, human fibroblasts, telomerase, DNA damage, serum deprivation, cell cycle arrest, tumor suppression
- MeSH terms
- Cell Line, DNA Damage, Fibroblasts, Gene Expression Regulation, Humans, Cellular Senescence, Telomerase, Genomics
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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