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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Authors | Zbigniew Polański, Hayden Homer, Jacek Z Kubiak |
Journal | Results and problems in cell differentiation
(Results Probl Cell Differ)
Vol. 55
Pg. 69-91
( 2012)
ISSN: 0080-1844 [Print] Germany |
PMID | 22918801
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- Cyclin B
- CDC2 Protein Kinase
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Topics |
- Animals
- CDC2 Protein Kinase
(metabolism)
- Cyclin B
(metabolism)
- Down Syndrome
(metabolism)
- Embryo, Mammalian
(metabolism)
- Embryonic Development
- Humans
- M Phase Cell Cycle Checkpoints
- Mice
- Oocytes
(metabolism)
- Proteolysis
- Trisomy
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