Parthenogenetic activation of oocytes in c-mos-deficient mice

TLDR: Results indicate that in mice Mos plays a role in the second meiotic metaphase arrest, but does not seem to be essential for the initiation of oocyte maturation, spermatogenesis or somatic cell cycle.

Abstract: IN Xenopus the c-mos proto-oncogene product (Mos) is essential for the initiation of oocyte maturation1, 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 function in mouse oocytes is unclear6–9, however, as is the biological significance of c-mos mRNA expression in testes1,10 and several somatic tissues1,10,11. We have generated c-mos-deficient mice by gene targeting in embryonic stem cells. These mice grew at the same rate as their wild-type counterparts and reproduction was normal in the males, but the fertility of the females was very low. The c-mos-deficient female mice developed ovarian teratomas at a high frequency. Oocytes from these females matured to the second meiotic metaphase both in vivo and in vitro, but were activated without fertilization. The results indicate that in mice Mos plays a role in the second meiotic metaphase arrest, but does not seem to be essential for the initiation of oocyte maturation, spermatogenesis or somatic cell cycle.