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Aging and p53: getting it straight A commentary on a recent paper by Gentry and Venkatachalam

Mice harboring the p53 ‘m’ allele – the result of a 0.6-Mb deletion affecting the p53 N-terminus as well as its upstream region – alongside a normal copy of the p53 gene, show decreased lifespan, premature aging and reduced cancer incidence. In the June issue of Aging Cell , Gentry and Venkatachalam provide a characterization of the entire m region, identifying 23 genes located upstream of p53. These authors propose that at least part if not all of the phenotype associated with the presence of the ‘m’ allele is caused by haploinsufficiency of one or more of the deleted genes and not by a truncated p53. We disagree with their interpretation and believe that the truncated p53 protein is the major, and likely the sole contributor, to both early aging and low cancer incidence in this mouse mutant. Tyner et al . (2002) previously described mice with a shortened lifespan, early onset of a number of normal aging symptoms and low cancer incidence. These mice were mutated for p53 by conventional gene targeting in embryonic stem cells. However, the mutation was anything but conventional. Somehow a large region of DNA was deleted such that the N-terminus of p53 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Aging Cell Wiley

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