Regulation of early embryo development: functional redundancy between cyclin subtypes

Cellular proliferation during early embryo development is achieved by the s erial cleavage of individual blastomeres into increasingly smaller cells, i n the absence of cell growth. This simplified cell division process has fac ilitated 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 ch aracteristics. For each of the A- and B-type cyclins, two subtypes have bee n identified so far in mammals. However, in both cases the two subtype gene s are expressed differentially, suggesting that they might have specific ro les. The requirement for individual cyclin A and B proteins during early mo use embryo development has been examined using gene-targeted deletion and i mmunofluorescence techniques. These studies have shown that cyclin A1 is no t essential for early embryonic development and cyclin A2 only becomes esse ntial for development beyond the stage of implantation. Cyclin B1 is also e ssential for development and its critical regulatory role during the meioti c 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.