Dear Editor,

Mutations in the p53 tumor suppressor gene are observed in up to 50% of all tumors and represent one of the most common genetic alterations in cancer. The high rate of spontaneous tumor development in p53-deficient mice was therefore not unexpected.1 However, considering the central role of p53 as a regulator of cellular proliferation and homeostasis, as well as cell death and premature senescence, the viability of p53 null mice and the abscence of developmental defects came as a surprise.1 Apart from neural tube closure defects in approximately 16% of female p53 null mice and a reduced reproductive capacity of both genders no in vivo developmental abnormalities have been reported.2 This is in striking contrast to the phenotype of p53 depletion in Xenopus embryos which leads to gastrulation failure and defects in mesoderm formation due to impaired TGF-β/Nodal/activin gene responses.3 A possible explanation for the different p53 knockout phenotype in Xenopus and mice is that p53 is only one member of a family of structurally and functionally related genes. In addition to p53, early mouse embryos express the p53 family members p63 and p73 that might compensate for the loss of p53, while in Xenopus p53 is solely responsible for early embryogenesis as p73 is not found in the lower vertebrates and Xenopus p63 is only expressed at later stages during organogenesis.3

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