Francoz Sarah, Froment Pascal, Bogaerts Sven, De Clercq Sarah, Maetens Marion, Doumont Gilles, Bellefroid Eric, Marine Jean-Christophe
Laboratory for Molecular Cancer Biology, Flanders Interuniversity Institute for Biotechnology, University of Ghent, Belgium.
Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3232-7. doi: 10.1073/pnas.0508476103. Epub 2006 Feb 21.
The Mdm2 and Mdm4 oncoproteins are key negative regulators of the p53 tumor suppressor. However, their physiological contributions to the regulation of p53 stability and activity remain highly controversial. Here, we combined a p53 knock-in allele, in which p53 is silenced by a transcriptional stop element flanked by loxP sites, with the mdm2- and mdm4-null alleles. This approach allows Cre-mediated conditional p53 expression in tissues in vivo and cells in vitro lacking Mdm2, Mdm4, or both. Using this strategy, we show that Mdm2 and Mdm4 are essential in a nonredundant manner for preventing p53 activity in the same cell type, irrespective of the proliferation/differentiation status of the cells. Although Mdm2 prevents accumulation of the p53 protein, Mdm4 contributes to the overall inhibition of p53 activity independent of Mdm2. We propose a model in which Mdm2 is critical for the regulation of p53 levels and Mdm4 is critical for the fine-tuning of p53 transcriptional activity, both proteins acting synergistically to keep p53 in check.
Mdm2和Mdm4癌蛋白是p53肿瘤抑制因子的关键负调控因子。然而,它们对p53稳定性和活性调控的生理作用仍极具争议。在此,我们将一个p53敲入等位基因(其中p53被两侧带有loxP位点的转录终止元件沉默)与mdm2和mdm4无效等位基因相结合。这种方法能够在体内组织和体外细胞中实现Cre介导的条件性p53表达,这些组织和细胞缺乏Mdm2、Mdm4或两者皆无。利用这一策略,我们表明Mdm2和Mdm4以非冗余方式对于在同一细胞类型中阻止p53活性至关重要,而与细胞的增殖/分化状态无关。尽管Mdm2可阻止p53蛋白的积累,但Mdm4独立于Mdm2对p53活性的全面抑制有贡献。我们提出一个模型,其中Mdm2对于p53水平的调控至关重要,而Mdm4对于p53转录活性的微调至关重要,这两种蛋白协同作用以控制p53。