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A p53-mediated DNA damage response limits reprogramming to ensure iPS cell genomic integrity
Open accessAbstract
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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“Many genetic abnormalities are found in human induced pluripotent stem (iPS) cells because early reprogramming of iPS cells triggers the DNA DSB response.(9,10) It will be very interesting to know whether D133p53 not only increases reprogramming efficiency by its antiapoptotic function, but also ensures genomic integr…”
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“Another intrinsic mechanism that protects the genome of HSC from damages caused by stress, radiation, and so forth, is the quiescent status of HSC, through an enhanced prosurvival gene expression and a strong activation of p53-mediated DNA damage repair responses, in which p21CipWaf1Sdi1 (p21) plays an important role…”
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Roles of p53 and ASF1A in the Reprogramming of Sheep Kidney Cells to Pluripotent Cells
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“Several groups identified the role of the p53 pathway in iPSC formation and found that inhibiting the p53 pathway dramatically increased the efficiency of iPSC generation (Hong et al., 2009; Kawamura et al., 2009; Li et al., 2009; Marión et al., 2009; Menendez et al., 2010; Spike and Wahl, 2011).”
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Glis1 and oxaloacetate in nucleus pulposus stromal cell somatic reprogramming and survival
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“P53, P21, and Ki67 transcripts levels agree with the concept of transcriptional activation of P21, leading to G1 arrest that would promote differentiation over proliferation, as in FAT cells reduced P21 expression upon lactic acid exposure correlated with increased Ki67 expression, indicating cell proliferation (Harad…”
BackgroundPapapetrou, E. P. (2017) · Advances in experimental medicine and biology · doi:10.1007/978-1-4939-7299-9_9 · Cited by 6
Correction: Telomere Reprogramming and Maintenance in Porcine iPS Cells
Ji, G., Ruan, W., Liu, K., Wang, F., Sakellariou, D., Chen, J., Yang, Y., Okuka, M., Han, J., Liu, Z., et al. (2013) · PLoS ONE · doi:10.1371/annotation/f5e4554b-18cc-46ef-ac39-73ac4d6750ae · Cited by 6
Inhibition of lung tumorigenesis by transient reprogramming in cancer cells
Pedrosa, P., Zhang, Z., Nuñez-Quintela, V., Macías, D., Ge, J., Denholm, M., Dyas, A., Estévez‐Souto, V., Lado‐Fernández, P., Gonzalez, P., et al. (2024) · Cell Death and Disease · doi:10.1038/s41419-024-07207-2 · Cited by 6
Comparative analysis of mouse strains for in vivo induction of reprogramming factors
Picó, S., Vílchez-Acosta, A., de Sousa, J. A., Maza, M. D. C. L., Mrabti, C., Parras, A., Desdín-Micó, G., Maroun, C. Y., Branchina, C., von Meyenn, F., et al. (2025) · Cell Reports · doi:10.1016/j.celrep.2025.115879 · Cited by 7
[Current progress and application prospects of induced pluripotent stem cells].
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McCaughey‐Chapman, A., Tarczyluk, M. A., Combrinck, C., Edwards, N., Jones, K., & Connor, B. J. (2023) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2023.1003188 · Cited by 7
“Multiple studies have previously shown that reprogramming of HDFs to hiPSCs resets aspects of cellular and molecular aging (Marión et al., 2009; Suhr et al., 2009, 2010; Horvath, 2013; Miller et al., 2013).”
BackgroundmTOR, autophagy, and reprogramming
Tang, B. L. (2014) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2013.00004 · Cited by 5
“Menendez and colleagues have argued that “forced expression of the Yamanaka cocktail of stemness factors is a stressful process that activates apoptosis and cellular senescence” (Menendez et al., 2011).”
BackgroundProgress and bottleneck in induced pluripotency
Zhang, Z., & Xu, Y. (2012) · Cell Regeneration · doi:10.1186/2045-9769-1-5 · Cited by 5
“While the impact of the transient silencing of p53 on the genomic stability of iPSCs remains to be examined, the iPSCs derived from p53 null cells exhibit extensive genomic instability [128].”
BackgroundPluripotency of Male Germline Stem Cells
Kim, S.-T., & Belmonte, J. C. I. (2011) · Molecules and Cells · doi:10.1007/s10059-011-1024-4 · Cited by 5
“The importance of p53 activity has been confirmed in a series of publications describing enhanced iPS formation by p53 knockout or knockdown, although SSC reprogramming may not always take the same route before pluripotency is achieved (Hong et al., 2009; Kawamura et al., 2009; Li et al., 2009; Marion et al., 2009; Ut…”
BackgroundGadd45a opens up the promoter regions of miR-295 facilitating pluripotency induction
Li, L., Chen, K., Wu, Y., Long, Q., Zhao, D., Ma, B., Pei, D., & Liu, X. (2017) · Cell Death and Disease · doi:10.1038/cddis.2017.497 · Cited by 5
“miR-34 is a target of P53, a known repressor of reprogramming.(17,19,20) miR-21 and miR-29a are abundantly”
BackgroundIshida, T., Ueyama, T., Ihara, D., Harada, Y., Nakagawa, S., Saito, K., Nakao, S., & Kawamura, T. (2023) · Biomedicines · doi:10.3390/biomedicines11061737 · Cited by 5
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Chang, B., Choi, Y., & Kim, J. (2015) · Journal of Reproduction and Development · doi:10.1262/jrd.2014-081 · Cited by 5
“A recent study [31] reported that inhibition of autophagy would increase the rate of apoptosis, which is another p53-regulated response to the overexpression of exogenous Yamanaka transcription factors that markedly decreases the efficiency of reprogramming.”
BackgroundConnecting the Cell Cycle with Cellular Identity
Chia, G., & Egli, D. M. (2013) · Cellular Reprogramming · doi:10.1089/cell.2013.0041 · Cited by 5
“…such as aging, extended culture in vitro (Atadja et al., 1995), cancer initiation (Serrano et al., 1997), aneuploidy (Thompson and Compton, 2010), and ectopic expression of transcription factors (Banito et al., 2009; Hong et al., 2009; Kawamura et al., 2009; Li et al., 2009; Marion et al., 2009).”
Tendency of K562 chronic myeloid leukemia cells towards cell reprogramming
Yılmazer, A. (2018) · Turkish Journal of Hematology · doi:10.4274/tjh.2018.0106 · Cited by 5
“On the other hand, expression of tumorsuppressor genes needs to be controlled during iPSC generation [15,18,19].”
BackgroundInduced Pluripotent Stem Cells
Okita, K., & Yamanaka, S. (2012) · Elsevier eBooks · doi:10.1016/b978-0-12-385942-6.00018-4 · Cited by 5
Yang, D., Guo, X., & Xi, R. (2025) · BioEssays · doi:10.1002/bies.70005 · Cited by 4
“Similarly, when intestinal stem cells (ISCs) are compromised by pathogen infection, differentiated intestinal cells such as enterocytes (ECs) or enteroendocrine cells (EECs) can dedifferentiate to replenish the ISC pool [8–10].”
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Scalf, S. M., Wu, Q., & Guo, S. (2025) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2025.102354 · Cited by 4
MDM4 enables efficient human iPS cell generation from PBMCs using synthetic RNAs
Nakagawa, M., Nogi, M., Doi, H., Hayashi, R., Katayama, T., Ohno, H., Mochizuki, M., Hayashi, K., & Saito, H. (2025) · Scientific Reports · doi:10.1038/s41598-025-16446-y · Cited by 4
Activation by ACA Induces Pluripotency in Human Blood Progenitor Cells
Becker-Kojić, Z. A., Ureña‐Peralta, J. R., Zipančić, I., Rodriguez-Jiménez, F. J., Rubio, M., Stojković, P., García-Roselló, M., & Stojković, M. (2013) · Bulletin of Experimental Biology and Medicine · doi:10.1007/s10517-013-2196-z · Cited by 4
Liu, X., Zhang, Y., Tong, M., Liu, X., Luo, G., Xie, D., Ren, S.-F., Bai, D., Wang, L., Zhou, Q., et al. (2013) · Acta Pharmacologica Sinica · doi:10.1038/aps.2013.61 · Cited by 4
Genetic and Epigenetic Instability of Human Pluripotent Stem Cells
Chung, T., Thakar, N. Y., & Wolvetang, E. (2011) · The Open Stem Cell Journal · doi:10.2174/1876893801103010052 · Cited by 53
“These observations indicate that during reprogramming, cells can 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 [33].”
BackgroundHu, W., Yan, Q., Yu, F., Qiu, Z., & Zhang, S. (2014) · Journal of Huazhong University of Science and Technology [Medical Sciences] · doi:10.1007/s11596-014-1249-5 · Cited by 4
Cai, Y., Dai, X. H., Zhang, Q., Hu, R., & Dai, Z. M. (2015) · Genetics and Molecular Research · doi:10.4238/2015.october.5.21 · Cited by 4
“…with the former studies that showed that the reprogramming process is somewhat similar to tumor development (Halazonetis et al., 2008; Kawamura et al., 2009; Marión et al., 2009; Utikal et al., 2009; Edel et al., 2010; Jasencakova and Groth, 2010; Menendez et al., 2010; Gupta et al., 2011).”
BackgroundGenomic Instability of Pluripotent Stem Cells: Origin and Consequences
Furno, E. L., van der Laan, S., & Maiorano, D. (2016) · InTech eBooks · doi:10.5772/62906 · Cited by 4
“Reprogramming increases γH2AX levels [78–80] and induces accumulation of genomic aberrancies ranging from whole chromosome aneuploidies, CNVs to point mutations [81], as well as epigenetic abnormalities [82].”
BackgroundPesaresi, M., Bonilla-Pons, S. A., & Cosma, M. P. (2018) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2018.07.002 · Cited by 4
Lenz, G. (2010) · Medical Hypotheses · doi:10.1016/j.mehy.2010.08.012 · Cited by 4
WDR36 Safeguards Self-Renewal and Pluripotency of Human Extended Pluripotent Stem Cells
An, S., Yao, D., Zhang, W., Sun, H., Yu, T., Ruizhe, J., & Yang, Y. (2022) · Frontiers in Genetics · doi:10.3389/fgene.2022.905395 · Cited by 4
Human Mutations Affecting Reprogramming into Induced Pluripotent Stem Cells
Hayashi, Y. (2017) · AIMS Cell and Tissue Engineering · doi:10.3934/celltissue.2017.1.31 · Cited by 4
“Also, fibroblasts from Atm -deficient mice showed remarkably low efficiency of iPSC generation compared to somatic cells from wild-type mice [13,24].”
Tsuda, Y., Tanikawa, C., Miyamoto, T., Hirata, M., Yodsurang, V., Zhang, Y., Imoto, S., Yamaguchi, R., Miyano, S., Takayanagi, H., et al. (2017) · Scientific Reports · doi:10.1038/s41598-017-11208-x · Cited by 4
Ohmine, S., Salisbury, J. L., Ingle, J. N., Pettinato, G., Haddox, C. L., Haddad, T. C., Galanis, E., Ikeda, Y., & D’Assoro, A. B. (2018) · Oncology Reports · doi:10.3892/or.2018.6239 · Cited by 4
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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