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    Phosphorylation of serine 18 regulates distinct p53 functions in mice

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    Authors
    Sluss, Hayla Karen
    Armata, Heather L.
    Gallant, Judith
    Jones, Stephen N.
    UMass Chan Affiliations
    Department of Cancer Biology
    Department of Cell Biology
    Document Type
    Journal Article
    Publication Date
    2004-01-20
    Keywords
    Animals
    Apoptosis
    Fibroblasts
    Mice
    *Nuclear Proteins
    Phosphorylation
    Phosphotransferases
    Proto-Oncogene Proteins
    Proto-Oncogene Proteins c-mdm2
    Sequence Analysis, DNA
    Serine
    Time Factors
    Tumor Suppressor Protein p53
    Life Sciences
    Medicine and Health Sciences
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    Abstract
    The p53 protein acts a tumor suppressor by inducing cell cycle arrest and apoptosis in response to DNA damage or oncogene activation. Recently, it has been proposed that phosphorylation of serine 15 in human p53 by ATM (mutated in ataxia telangiectasia) kinase induces p53 activity by interfering with the Mdm2-p53 complex formation and inhibiting Mdm2-mediated destabilization of p53. Serine 18 in murine p53 has been implicated in mediating an ATM- and ataxia telangiectasia-related kinase-dependent growth arrest. To explore further the physiological significance of phosphorylation of p53 on Ser18, we generated mice bearing a serine-to-alanine mutation in p53. Analysis of apoptosis in thymocytes and splenocytes following DNA damage revealed that phosphorylation of serine 18 was required for robust p53-mediated apoptosis. Surprisingly, p53Ser18 phosphorylation did not alter the proliferation rate of embryonic fibroblasts or the p53-mediated G(1) arrest induced by DNA damage. In addition, endogenous basal levels and DNA damage-induced levels of p53 were not affected by p53Ser18 phosphorylation. p53Ala18 mice developed normally and were not susceptible to spontaneous tumorigenesis, and the reduced apoptotic function of p53Ala18 did not rescue the embryo-lethal phenotype of Mdm2-null mice. These results indicate that phosphorylation of the ATM target site on p53 specifically regulates p53 apoptotic function and further reveal that phosphorylation of p53 serine 18 is not required for p53-mediated tumor suppression.
    Source
    Mol Cell Biol. 2004 Feb;24(3):976-84.
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/38557
    PubMed ID
    14729946
    Related Resources
    Link to Article in PubMed
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    UMass Chan Faculty and Researcher Publications

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