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The tumor suppressor gene p53, which is the most frequently mutated gene in human tumors, controls cell cycle checkpoint and apoptosis via the transactivation of the transcription of a collection of genes. These activities avoid proliferation of cell bearing alteration of genetic material. However, like a two-edged sword, p53 can also directly participate to genome stability maintenance by repressing homologous recombination (HR), independently of the transactivation activity. This parallel activity allows to limit the deleterious consequences on an excess of HR. Beside genetic interactions, p53 protein physically interacts with both HR proteins and HR intermediates (heteroduplex and Holliday junctions). The core domain of p53 is required for interaction with Rad51 at an early step and the carboxy-terminal domain of p53 is involved in the interaction with Rad54 and HR intermediates, at a late step. We discuss here the putative consequences of this parallel activity of p53 on genome stability, speciation and tumor protection.

Rôle direct dep53dans la recombinaison homologue