We previously showed that ATM is responsible for p53 phosphorylation at Ser15 andlocalization at centrosomes during mitosis. When p53 centrosomal localization is preventedby inhibiting polymerization of spindle microtubules, a stabilized form of p53 is transmittedto daughter cells that arrest in the next G1 phase of the cell cycle after exit from mitosis. ATcells are unable to both localize p53 at centrosomes in mitosis and arrest after exposure tomitotic-spindle poisons. Here we show that during mitosis ATM is activated byphosphorylation at Ser1981 and localizes at centosomes. When mitotic spindle is disrupted bynocodazole, ATM is displaced from centrosomes and co-localizes with phospho-Ser15-p53under the form of spots dispersed in the mitotic cytoplasm. After release from nocodazoleblock,as soon as cells exit mitosis, p53 is redirected to the nucleus and its Ser15phosphorylation is substituted by phosphorylation at Ser46. We suggest that ATM is activatedby default at each mitotic onset and phosphorylates p53 at Ser15 so as to keep it inactive atcentrosomes when the spindle is correctly in place or, in case of inactivation of the mitoticspindle, to maintain the memory of a perturbed mitosis.