Chapter

Mouse Development

Volume 55 of the series Results and Problems in Cell Differentiation pp 69-91

Date:

Cyclin B in Mouse Oocytes and Embryos: Importance for Human Reproduction and Aneuploidy

  • Zbigniew PolańskiAffiliated withDepartment of Genetics and Evolution, Institute of Zoology, Jagiellonian University
  • , Hayden HomerAffiliated withMammalian Oocyte and Embryo Research Laboratory, Institute for Women’s Health, University College London and University College London Hospitals NHS Foundation TrustDepartment of Obstetrics and Gynaecology, Institute for Women’s Health, University College London and University College London Hospitals NHS Foundation Trust
  • , Jacek Z. KubiakAffiliated withInstitut de Génétique et Développement de Rennes, CNRS, UMR 6290IFR 140, Faculté de Médecine, Université Rennes 1, UEB Email author 

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Abstract

Oocyte maturation and early embryo development require precise coordination between cell cycle progression and the developmental programme. Cyclin B plays a major role in this process: its accumulation and degradation is critical for driving the cell cycle through activation and inactivation of the major cell cycle kinase, CDK1. CDK1 activation is required for M-phase entry whereas its inactivation leads to exit from M-phase. The tempo of oocyte meiotic and embryonic mitotic divisions is set by the rate of cyclin B accumulation and the timing of its destruction. By controlling when cyclin B destruction is triggered and by co-ordinating this with the completion of chromosome alignment, the spindle assembly checkpoint (SAC) is a critical quality control system important for averting aneuploidy and for building in the flexibility required to better integrate cell cycle progression with development. In this review we focus on cyclin B metabolism in mouse oocytes and embryos and illustrate how the cell cycle-powered clock (in fact cyclin B-powered clock) controls oocyte maturation and early embryo development, thereby providing important insight into human reproduction and potential causes of Down syndrome.