Dear Editor,

Members of the p53 family of transcription factors, including p63 and p73, play distinct roles in tumor suppression and development. p53 plays a prominent role in tumor suppression, as indicated by the high frequency of p53 mutations found in human cancer and by the fact that p53-deficient mice are highly cancer prone.1 In contrast, while some evidence indicates a role for p63 and p73 in tumor suppression,2 the best characterized functions of the p63 and p73 proteins are in development. p73−/− mice are prone to lethal infections, as well as abnormalities in brain development and pheromone sensing, while p63−/− mice fail to develop skin, oral epithelia, or other ectoderm-derived appendages.1 Mutations in p63 also have been identified in multiple human ectodermal dysplasia syndromes, in which patients display abnormal development of ectoderm-derived tissues, including the skin, teeth, hair, and nails, along with other symptoms.1 Recent studies suggest further that loss of p63 in the stratified epithelia of adult mice results in cellular senescence and premature organismal aging.3 Together these findings underscore the pivotal role of p63 in the proper development and function of ectoderm-derived tissues. However, the mechanisms by which p63 acts remain largely unknown, as few direct target genes mediating p63 function in epithelia have been identified. Like the transcription factors that direct their expression, p53/p63 target genes might also be candidates for mutation in diseases affecting tissue homeostasis, aging, or tumor suppression in the adult organism.

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