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Genetic Interactions between the Wilms’ Tumor 1 Gene and the p53 Gene¹

Central Hematologie Laboratory, University Medical Centre St. Radboud, 6500 HB, Nijmegen, the Netherlands [A. L. M.]; Medical Research Council Human Genetics Unit, Western General Hospital, EH4 2XU, Edinburgh, United Kingdom [A. L., A. I., K. A. W., L. S., N. D. H.]; Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3US, United Kingdom [A. R. C.]; and Department of Pathology, University Medical School, Edinburgh, EH8 9AG, United Kingdom [D. J. H.]

In recent years, a number of proteins have been identified that can modify the activities of the Wilms’ Tumor 1 (WT1) proteins. One of these modifiers is the p53 protein. To investigate a genetic interaction between the p53 gene and the wt1 gene, we have crossed their respective knockout mice. The absence of p53 appears to have no gross effect on the phenotype of wt1-null mice. Both wt1-null and double-null embryos develop pericardial bleeding and die in utero. In adult p53-null mice, wt1-heterozygosity (wt1het) predisposes to an earlier onset of lymphomagenesis and the development of kidney abnormalities resembling oncocytoma in humans. wt1-heterozygosity alone predisposes to the development of glomerular sclerosis.

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