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A p53-mediated DNA damage response limits reprogramming to ensure iPS cell genomic integrity
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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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“In agreement with the negative role of prolonged p53 expression on stem cell potency, it was shown that p53 restricted the stem cell gene expression program [69].”
From Ultraviolet Radiation‐Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging (2016) · cites this paper as [69]
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The Secret Lives of Pluripotent Cells: There and Back Again
Cinelli, P. (2010) · Genes · doi:10.3390/genes1010004 · Cited by 1
“Recent data indicated that cells undergoing reprogramming experience yet uncharacterized genotoxic stress [13], similar to that shown for oncogene activation in both in vitro and in vivo systems [14-16].”
BackgroundThe role of cell cycle in reprogramming toward induced pluripotent stem cells (iPSCs)
Neganova, I. E. (2021) · Elsevier eBooks · doi:10.1016/b978-0-323-90059-1.00015-4 · Cited by 1
Induced Pluripotent Stem Cells
Yoshida, Y., & Yamanaka, S. (2013) · CRC Press eBooks · doi:10.1201/b14990-2 · Cited by 1
The Role of Stem Cell Genomic Instability in Aging
Sieben, C. J., Childs, B. G., & Baker, D. J. (2015) · Current Stem Cell Reports · doi:10.1007/s40778-015-0020-6 · Cited by 1
Therapeutic Possibilities of Induced Pluripotent Stem Cells
Ayetey, H. (2010) · Stem cell biology and regenerative medicine · doi:10.1007/978-1-60761-959-8_8 · Cited by 1
Stem Cells and Parkinson's Disease
Lane, E. L., Sundberg, M., & Pruszak, J. (2012) · Wiley-VCH eBooks · doi:10.1002/3527600906.mcb.201100019 · Cited by 1
The role of polyhomeotic in polycomb group-mediatedregulation of the tumour suppressor P16INK4A
de Breed, L. A. (2010) · UCL Discovery (University College London) · Cited by 1
Revisiting the canonical tumour progression model
Ansieau, S., Hinkal, G. W., Morel, A., & Puisieux, A. (2010) · Pathologie Biologie · doi:10.1016/j.patbio.2009.11.005 · Cited by 1
Is the Perfect Mouse Cloning Experiment in Sight?
Boiani, M. (2010) · Biology of Reproduction · doi:10.1095/biolreprod.110.088310 · Cited by 1
“The connection to apoptosis presents an interesting similarity with the case of iPS reprogramming, where TRP53 inhibition increases reprogramming rates as measured by the frequency of alkaline phosphatase þ , NANOG þ , or POU5F1(OCT4) þ colonies [27, 28].”
BackgroundBaker, M. (2009) · Nature reports. Stem cells · doi:10.1038/stemcells.2009.132 · Cited by 1
Womack, J. E. (2010) · ILAR Journal · doi:10.1093/ilar.51.1.85 · Cited by 1
Induced Pluripotent Stem Cells and the Promise of Proliferation
Williams, R. (2009) · Circulation Research · doi:10.1161/circresaha.109.211250 · Cited by 1
The Progress of Induced Pluripotent Stem Cells (iPSCs) for Research and Applications
Fu, Y., Zhou, X., Feng-qing, X. U., & Qian, Q. (2011) · PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS · doi:10.3724/sp.j.1206.2010.00333 · Cited by 1
Micropatterned substrates to promote and dissect reprogramming of human somatic cellsPreprint
Carlson-Stevermer, J., Harkness, T., Prestil, R., Seymour, S. K., Knight, G. T., Ashton, R. S., & Saha, K. (2017) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/111369 · Cited by 1
“This higher proliferation rate could be due to the activity of reprogramming factors driving cell cycle progression as previously noted (Hanna et al., 2009; Kawamura et al., 2009; Marión et al., 2009).”
BackgroundBalancing dynamic tradeoffs drives cellular reprogrammingPreprint
Babos, K. N., Galloway, K. E., Kisler, K., Zitting, M., Li, Y., Quintino, B., Chow, R. H.-P., Zloković, B. V., & Ichida, J. K. (2018) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/393934 · Cited by 1
“Although lineage conversion into somatic lineages is becoming increasingly desirable for translational studies, efforts to identify mechanisms that limit transcription factor-mediated lineage conversion have focused primarily on iPSC generation (8-15).”
BackgroundNon-cell-autonomous promotion of pluripotency induction mediated by YAPPreprint
Hartman, A. A., Hu, X., Chen, X., Eastman, A. E., Yang, C. L.-H., & Guo, S. (2018) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/481127 · Cited by 1
“…(Mosteiro et al., 2016; Mosteiro et al., 2018), but the senescent cells themself are inefficient in reprograming (Banito et al., 2009; Hanna et al., 2009; Hong et al., 2009; Kawamura et al., 2009; Li et al., 2009; Marion et al., 2009; Park et al., 2008; Utikal et al., 2009; Zhao et al., 2008).”
Background
Metadata
- 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)
- Venue
- Nature
- Published
- 2009-08
- Volume
- 460
- Issue
- 7259
- Pages
- 1149-1153
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- 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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