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Regulation of early embryo development: functional redundancy between cyclin subtypes.

Cellular proliferation during early embryo development is achieved by the serial cleavage of individual blastomeres into increasingly smaller cells, in the absence of cell growth. This simplified cell division process has facilitated the study of the cell cycle and its regulatory pathways. The cell cycle of mammalian cells is controlled by a number of mechanisms, including the activity of cyclin-dependent protein kinase complexes. Numerous cyclin proteins have been identified and these share structural and functional characteristics. For each of the A- and B-type cyclins, two subtypes have been identified so far in mammals. However, in both cases the two subtype genes are expressed differentially, suggesting that they might have specific roles. The requirement for individual cyclin A and B proteins during early mouse embryo development has been examined using gene-targeted deletion and immunofluorescence techniques. These studies have shown that cyclin A1 is not essential for early embryonic development and cyclin A2 only becomes essential for development beyond the stage of implantation. Cyclin B1 is also essential for development and its critical regulatory role during the meiotic maturation of mouse oocytes will be considered. This review will discuss the studies that have attempted to explain the possible redundancy between the different cyclin subtypes.