Abstract
In mammalian cells, the p53 protein is a key regulator of the cell cycle following DNA damage. In the present study, we investigated the function of p53 in the A6 amphibian cell line. Using various specific Xenopus p53 monoclonal antibodies, we showed that Xenopus p53 accumulates after DNA damage, including gamma and UV irradiation or treatment with adriamycin. Such accumulation is accompanied by an increase in the apparent molecular weight of the protein. This change was shown to be the result of a phosphorylation event that occurs after DNA damage. Accumulation of Xenopus p53 is parallel to a drastic change in the cell cycle distribution. Brief exposure to adriamycin or gamma irradiation induces reversible growth arrest, whereas long-term exposure to adriamycin leads to apoptosis. Taken together, these results indicate that p53 has a similar behaviour in frog cells and mammalian cells, and that it conserves two activities, cell cycle arrest and apoptosis.
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Acknowledgements
We thank J Bram, M Le Bras, Z Macïorowski and G Zalcman for critical reading of the manuscript. This work was supported by grants from the Ligue Nationale contre le Cancer (Comité de Paris) and the Association pour la Recherche contre le Cancer (ARC). K Bensaad is supported by a fellowship from the Ligue Nationale contre le Cancer (Comité National).
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Bensaad, K., Rouillard, D. & Soussi, T. Regulation of the cell cycle by p53 after DNA damage in an amphibian cell line. Oncogene 20, 3766–3775 (2001). https://doi.org/10.1038/sj.onc.1204492
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DOI: https://doi.org/10.1038/sj.onc.1204492
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