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

Rosa M. Marión, Katerina Strati, Han Li, Matilde Murga, Raquel Blanco, Sagrario Ortega, Oscar Fernandez-Capetillo, Manuel Serrano and Maria A. Blasco ()
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Rosa M. Marión: Telomeres and Telomerase Group,
Katerina Strati: Telomeres and Telomerase Group,
Han Li: Tumor Suppression Group,
Matilde Murga: Genetic Instability Group, Molecular Oncology Program, Spanish National Cancer Research Centre (CNIO), Melchor Fernández Almagro 3, Madrid E-28029, Spain
Raquel Blanco: Telomeres and Telomerase Group,
Sagrario Ortega: Transgenic mice Unit, Biotechnology Program, Spanish National Cancer Research Centre (CNIO), Melchor Fernández Almagro 3, Madrid E-28029, Spain
Oscar Fernandez-Capetillo: Genetic Instability Group, Molecular Oncology Program, Spanish National Cancer Research Centre (CNIO), Melchor Fernández Almagro 3, Madrid E-28029, Spain
Manuel Serrano: Tumor Suppression Group,
Maria A. Blasco: Telomeres and Telomerase Group,

Nature, 2009, vol. 460, issue 7259, 1149-1153

Abstract: On iPS cells and p53: reprogramming DNA damage responses Marión et al. show that p53 is critically involved in preventing the reprogramming of cells carrying various types of DNA damage, including short telomeres, DNA repair deficiencies, or with exogenously inflicted DNA damage. Eliminating p53 expression allows efficient reprogramming in the face of DNA damage and the generation of iPS cells carrying persistent DNA damage and chromosomal aberrations. They conclude that p53 is critical in preventing the generation of pluripotent cells from suboptimal parental cells.

Date: 2009
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DOI: 10.1038/nature08287

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