Introduction

An ordered series of molecular events in somatic cells ensures that DNA replication during S phase occurs before the segregation of sister chromatids at anaphase (see Murray and Hunt, 1993). The processes that control and monitor the two sequential but biochemically unrelated events of replication and segregation have been termed cell cycle checkpoints by Hartwell and Weinert (1989). These mechanisms survey cells for a series of events including replication, DNA damage, spindle assembly and chromatid segregation and act as guardians of cell cycle fidelity. Defects in this intricate series of checkpoints not only have catastrophic effects on cell division but have also been directly implicated in the generation of cancer (Murray, 1992; Hartwell et al, 1997).

The growing oocyte is incapable both of completing meiosis and of supporting early embryonic development. Even after the completion of the growth phase, the oocyte remains unable to support development until it has completed a final phase of differentiation. This phase, the so-called oocyte maturation, involves both nuclear and cytoplasmic components, the biochemistry of which are described in earlier chapters of this book. The endpoint of maturation is the production of an oocyte, arrested at the metaphase II stage of meiosis, but possessing the full competence after fertilization of supporting normal embryonic development. The efficiency of this maturation process varies from very high rates in many rodents and ungulates to disappointing low rates in humans. Two questions are raised by these facts: why is the efficiency of human reproduction so exceptionally low (Grobstein, 1979) and what checkpoint mechanisms exist to prevent cell cycle progression in oocytes and embryos that carry abnormalities? It is with this latter question that this chapter is concerned.

That checkpoint controls in meiotic cells might differ in important respects from those that operate during mitosis is evident from the differing nature of the two types of cell cycle (Dai et al., 2000). From a checkpoint control perspective, meiosis is unique because of the occurrence of meiotic recombination during the early G2 phase, the absence of sister chromatid separation during anaphase I and the direct progression from one M phase to a second M phase with no intervening S phase.