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.
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While writing this article, JZK was supported by a grant from ARC. HH is supported by a Wellcome Trust Fellowship. ZP was supported by the Polish National Science Centre (grant N° DEC-2011/B/NZ3/00190).
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Polański, Z., Homer, H., Kubiak, J.Z. (2012). Cyclin B in Mouse Oocytes and Embryos: Importance for Human Reproduction and Aneuploidy. In: Kubiak, J. (eds) Mouse Development. Results and Problems in Cell Differentiation, vol 55. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-30406-4_4
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