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p63 null mutation protects mouse oocytes from radio-induced apoptosis

¹ CEA, DSV/DRR/SEGG/LDRG, Unit of Gametogenesis and Genotoxicity, Laboratory of Differentiation and Radiobiology of the Gonads, F-92265 Fontenay aux Roses, France² Univ Paris 7-Denis Diderot, UFR of Biology, UMR-S 566, F-92265 Fontenay aux Roses, France and³ INSERM, U566, F-92265 Fontenay aux Roses, France

Correspondence should be addressed to G Livera at Unit of Gametogenesis and Genotoxicity, CEA, Université Paris 7, INSERM U566, CEA/DSV/DRR/SEGG/LDRG, Route du Panorama-BP6, 92265 Fontenay aux Roses Cedex, France; Email: gabriel.livera{at}cea.fr

Female fertility in mammals is determined by the pool of primordial follicles and low doses of radiation induce a major loss of primordial follicles in the ovary. We investigated the expression of p53 and its homologues, p63 and p73, in the normal and irradiated neonatal ovary. p63 was the only member of the p53 family detected in oocyte nucleus. No p63 transcripts or protein were detected in the early foetal ovary. p63 production began in late pachytene-stage oocytes and peaked in diplotene oocytes in mice and humans. The production of p63 was correlated with meiotic DNA double-strand break repair. Only transactivation (TA) isoforms were present in the ovary, with TAp63 by far the most abundant in terms of mRNA and protein levels. Complete p63 null mutation did not affect normal ovary development. Irradiation rapidly triggered p63 phosphorylation. p63 null mutation prevented the cleavage of caspases-9 and -3 and the follicle loss induced by ionising radiation. Thus, our results evidence that irradiation-induced depletion of the primordial follicle pool results from the activation of p63 in quiescent oocytes.