p63 null mutation protects mouse oocytes from radio-induced apoptosis

International audienceFemale fertility in mammals is determined by the pool of primordial follicles and low doses of radiation induce a major loss of primordialfollicles in the ovary. We investigated the expression of p53 and its homologues, p63 and p73, in the normal and irradiated neonatalovary. p63 was the only member of the p53 family detected in oocyte nucleus. No p63 transcripts or protein were detected in the earlyfoetal ovary. p63 production began in late pachytene-stage oocytes and peaked in diplotene oocytes in mice and humans. The productionof p63 was correlated with meiotic DNA double-strand break repair. Only transactivation (TA) isoforms were present in the ovary, withTAp63$\alpha$ by far the most abundant in terms of mRNA and protein levels. Complete p63 null mutation did not affect normal ovarydevelopment. Irradiation rapidly triggered p63 phosphorylation. p63 null mutation prevented the cleavage of caspases-9 and -3 and thefollicle loss induced by ionising radiation. Thus, our results evidence that irradiation-induced depletion of the primordial follicle poolresults from the activation of p63 in quiescent oocytes