PARTHENOGENETIC ACTIVATION OF OOCYTES IN C-MOS-DEFICIENT MICE

IN Xenopus the c-mos proto-oncogene product (Mos) is essential for the initiation of oocyte maturation(1), for the progression from meiosis I to meiosis II2,3 and for the second meiotic metaphase arrest, acting as an essential component of the cytostatic factor CSF4,5. Its functi on in mouse oocytes is unclear(6-9), however, as is the biological sig nificance of c-mos mRNA expression in testes(1,10) and several somatic tissues(1,10,11). We have generated c-mos-deficient mice by gene targ eting in embryonic stem cells. These mice grew at the same rate as the ir wild-type counterparts and reproduction was normal in the males, bu t the fertility of the females was very low. The c-mos-deficient femal e mice developed ovarian teratomas at a high frequency. Oocytes from t hese females matured to the second meiotic metaphase both in vivo and in vitro, but were activated without fertilization. The results indica te that in mice Mos plays a role in the second meiotic metaphase arres t, but does not seem to be essential for the initiation of oocyte matu ration, spermatogenesis or somatic cell cycle.