Cited by 1,028Pluripotent Stem Cells ResearchTelomeres, Telomerase, and SenescenceDNA Repair Mechanisms

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A p53-mediated DNA damage response limits reprogramming to ensure iPS cell genomic integrity

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Marión, Rosa M., Strati, Katerina, Li, Han, Murga, Matilde, Blanco, Raquel, Ortega, Sagrario, Fernandez-Capetillo, Oscar, Serrano, Manuel, Blasco, Maria A.·2009·Nature

DOI 10.1038/nature08287PMC PMC3624089

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Abstract

The reprogramming of differentiated cells to pluripotent cells (induced pluripotent stem (iPS) cells) is known to be an inefficient process. We recently reported that cells with short telomeres cannot be reprogrammed to iPS cells despite their normal proliferation rates, probably reflecting the existence of 'reprogramming barriers' that abort the reprogramming of cells with uncapped telomeres. Here we show that p53 (also known as Trp53 in mice and TP53 in humans) is critically involved in preventing the reprogramming of cells carrying various types of DNA damage, including short telomeres, DNA repair deficiencies, or exogenously inflicted DNA damage. Reprogramming in the presence of pre-existing, but tolerated, DNA damage is aborted by the activation of a DNA damage response and p53-dependent apoptosis. Abrogation of p53 allows efficient reprogramming in the face of DNA damage and the generation of iPS cells carrying persistent DNA damage and chromosomal aberrations. These observations indicate that during reprogramming cells increase their intolerance to different types of DNA damage and that p53 is critical in preventing the generation of human and mouse pluripotent cells from suboptimal parental cells.

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Peer Review #1 of "Ten years of progress and promise of induced pluripotent stem cells: historical origins, characteristics, mechanisms, limitations, and potential applications (v0.1)"
(2018) · PeerJ · doi:10.7287/peerj.4370v0.1/reviews/1
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Attenuating iPSC Reprogramming Stresses with Dominant Negative BET PeptidesPreprint
Hossain, M. E., Cevallos, R. R., Zhang, R., & Hu, K. (2022) · SSRN Electronic Journal · doi:10.2139/ssrn.4175581
Modulating the epigenetic state promotes the reprogramming of transformed cells to pluripotency in a line-specific mannerPreprint
Fu, X., Zhuang, Q., Babarinde, I. A., Shi, L., Ma, G., Hu, H., Li, Y., Chen, J., Xiao, Z., Deng, B., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.12.01.518778
“Loss of p53 is beneficial for reprogramming in wildtype cells 245 [40, 53, 54], yet in transformed lines reduced p53 activity in the p53DD.”
Background
Effect of doxorubicin on viability and Bax, Bcl-2, p53, Nanog, Sox-2, Oct-4 gene expressions in MCF-7 stem-like cellsPreprint
Andac, C. A., Koçak, N., Dalan, A. B., Çağlar-Andac, S., & Arslan, S. O. (2023) · Research Square · doi:10.21203/rs.3.rs-2677263/v1
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Fujii, Y. R. (2023) · Springer eBooks · doi:10.1007/978-981-99-3165-1_9
Failed reprogramming of transformed cells due to induction of apoptosis and senescence impairs tumor progression in lung cancerPreprint
Pedrosa, P., Zhang, Z., Macías, D., Ge, J., Denholm, M., Dyas, A., Nuñez-Quintela, V., Estévez‐Souto, V., Lado‐Fernández, P., Gonzalez, P., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.10.19.563086

Authors: Marión, R. M., Strati, K., Li, H., Murga, M., Blanco, R., Ortega, S., Fernandez-Capetillo, O., Serrano, M., & Blasco, M. A.
Affiliations: Spanish National Cancer Research Centre (ES)
ORCID: Strati, Katerina
Li, Han
Murga, Matilde
Blanco, Raquel
Ortega, Sagrario
Serrano, Manuel
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2009-08
Volume: 460
Issue: 7259
Pages: 1149-1153
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/nature08287
PMC: PMC3624089
OpenAlex: W2111920812
Cited by: 1,028
References: 29
Citations by year: 2026: 12 · 2025: 20 · 2024: 13 · 2023: 20 · 2022: 37 · 2021: 24 · 2020: 35 · 2019: 45 · 2018: 46 · 2017: 51 · 2016: 60 · 2015: 72 · 2014: 84 · 2013: 110 · 2012: 135
FWCI: 53.60
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
RePEc: Research Papers in Economics (submittedVersion)
Funders: Ministerio de Ciencia e Innovación
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Keywords: p53, DNA damage response, induced pluripotent stem cells, cellular reprogramming, short telomeres, DNA repair deficiency, chromosomal abnormalities, genome stability, apoptosis, pluripotency
MeSH terms: Animals, Cells, Cultured, Chromosome Aberrations, DNA Damage, DNA Repair, Female, Fibroblasts, Humans, Male, Tumor Suppressor Protein p53, Telomere, Apoptosis, Pluripotent Stem Cells, Genomic Instability, Mice, Cellular Reprogramming

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A p53-mediated DNA damage response limits reprogramming to ensure iPS cell genomic integrity

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