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EMBO reports 7, 5, 546–552 (2006)
doi:10.1038/sj.embor.7400667
AOP Published online: 31 March 2006
Increased p53 activity does not accelerate telomere-driven ageing
Isabel García-Cao1, Marta García-Cao2, Antonia Tomás-Loba2, Juan Martin-Caballero3, Juana M Flores4, Peter Klatt1, 2, María A Blasco2 & Manuel Serrano1
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1 Tumor Suppression Group
2 Telomeres and Telomerase Group
3 Animal Facility Unit, Spanish National Cancer Center (CNIO), 3 Melchor Fernández Almagro Street, Madrid 28029, Spain
4 Department of Animal Surgery and Medicine, Veterinary School, Complutense University, Madrid 28040, Spain
To whom correspondence should be addressed
Manuel Serrano Tel: +34 917 328 032; Fax: +34 917 328 028; E-mail: mserrano@cnio.es
Received 28 September 2005; Accepted 28 February 2006; Published online 31 March 2006.
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Abstract
There is a great interest in determining the impact of p53 on ageing and, for this, it is important to discriminate among the known causes of ageing. Telomere loss is a well-established source of age-associated damage, which by itself can recapitulate ageing in mouse models. Here, we have used a genetic approach to interrogate whether p53 contributes to the elimination of telomere-damaged cells and its impact on telomere-driven ageing. We have generated compound mice carrying three functional copies of the p53 gene (super-p53) in a telomerase-deficient background and we have measured the presence of chromosomal abnormalities and DNA damage in several tissues. We have found that the in vivo load of telomere-derived chromosomal damage is significantly decreased in super-p53/telomerase-null mice compared with normal-p53/telomerase-null mice. Interestingly, the presence of extra p53 activity neither accelerates nor delays telomere-driven ageing. From these observations, we conclude that p53 has an active role in eliminating telomere-damaged cells, and we exclude the possibility of an age-promoting effect of p53 on telomere-driven ageing.
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