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Explaining the biological activity of transactivation-deficient p53 variants

Nature Genetics volume 38, pages 395–396 (2006)Cite this article

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To the Editor:

Johnson et al.1 recently reported a conditional mouse Trp53 allele with mutations changing codons 25 and 26 to glutamine and serine, respectively (referred to below as Trp53QS). These mutations largely disable p53 transactivation function. Surprisingly, heterozygosity for Trp53QS caused embryonic lethality.

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Figure 1: Trp53QS knock-in MEFs express substantially more p53 protein than Trp53QS-Val135 knock-in MEFs but show similar regulation of p53 target genes.

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Authors and Affiliations

  1. The Salk Institute for Biological Studies, Gene Expression Laboratory, 10010 N. Torrey Pines Road, La Jolla, 92037, California, USA

    Mengjia Tang & Geoffrey M Wahl

  2. Department of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Stockholm, 171 76, Sweden

    Monica Nistér

  3. Department of Genetics and Pathology, Rudbeck Laboratory, University of Uppsala, Uppsala, 751 85, Sweden

    Monica Nistér

Authors
  1. Mengjia Tang
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  2. Geoffrey M Wahl
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  3. Monica Nistér
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Tang, M., Wahl, G. & Nistér, M. Explaining the biological activity of transactivation-deficient p53 variants. Nat Genet 38, 395–396 (2006). https://doi.org/10.1038/ng0406-395

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