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Disruption of c-mos causes parthenogenetic development of unfertilized mouse eggs

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Abstract

THE c-mos proto-oncogene encodes a 37-39K cytoplasmic serine/ threonine kinase1 implicated in the meiotic maturation events during murine spermatogenesis2 and oogenesis3–6. In Xenopus, ectopic expression of pp39mos can promote both the meiotic matur-ation of oocytes7–9 and also arrest the cleavage of blastomeres10. To elucidate the role of pp39mos we have generated homozygous mutant mice by gene targeting in embryonic stem cells11. These mice are viable and mutant males are fertile, demonstrating that pp39mos is not essential for spermatogenesis. In contrast, mutant females, have a reduced fertility because of the failure of mature eggs to arrest during meiosis. c-mos-/- oocytes undergo germinal vesicle breakdown and extrusion of both polar bodies followed in some cases by progression into cleavage. Mutant females also develop ovarian cysts. These results demonstrate that a major role for pp39mos is to prevent the spontaneous parthenogenetic activation of unfertilized eggs.

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Author notes

  1. G. B. Udy: AgResearch, Molecular Embryology, Ruakura Agricultural Centre, Private Bag 3123, Hamilton, New Zealand

Authors and Affiliations

  1. Wellcome/CRC Institute of Cancer and Developmental Biology, and Department of Genetics, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QR, UK

    W. H. Colledge, M. B. L. Carlton, G. B. Udy & M. J. Evans

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  1. W. H. Colledge
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  2. M. B. L. Carlton
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  3. G. B. Udy
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  4. M. J. Evans
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Colledge, W., Carlton, M., Udy, G. et al. Disruption of c-mos causes parthenogenetic development of unfertilized mouse eggs. Nature 370, 65–68 (1994). https://doi.org/10.1038/370065a0

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