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Reply to Explaining the biological activity of transactivation-deficient p53 variants

Nature Genetics volume 38, pages 396–397 (2006)Cite this article

In reply:

Our laboratory recently generated conditional Trp53 knock-in mice in which codons 25 and 26 were mutated to glutamine and serine (QS) to address the role of transactivation in p53 function1. Our Trp53QS mice have a different phenotype from those described by Wahl and colleagues2, which also carry a mutation in the DNA binding domain at codon 135 (Trp53QS-Val135)3. Our analysis of Trp53QS mice demonstrates that this mutant retains select p53 activities. In contrast, Wahl and colleagues show that the Trp53QS-Val135 allele behaves indistinguishably from a Trp53-null allele.

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Figure 1: p53QS does not hyperactivate wild-type p53.

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Author information

Authors and Affiliations

  1. Department of Radiation Oncology, Stanford University School of Medicine, Stanford, 94305, California, USA

    Thomas M Johnson

  2. Departments of Radiation Oncology and Genetics, Stanford University School of Medicine, Stanford, 94305, California, USA

    Laura D Attardi & Laura D Attardi

Authors
  1. Thomas M Johnson
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  2. Laura D Attardi
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Supplementary information

Supplementary Fig. 1

p53 QS-wt effects on embryogenesis in relation to wild-type p53 (PDF 320 kb)

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Johnson, T., Attardi, L. Reply to Explaining the biological activity of transactivation-deficient p53 variants. Nat Genet 38, 396–397 (2006). https://doi.org/10.1038/ng0406-396

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