Cdk1 drives meiosis and mitosis through two different mechanisms

Cell cycle progression in mammals involves multiple cyclin-dependent kinases (Cdks). Mice lacking Cdk2, Cdk3, Cdk4 or Cdk6 are viable, however, because Cdk1 can compensate for their loss by forming active complexes with A-, B-, Eand D-type cyclins in a stepwise manner. Thus, these Cdks are not essential for the mammalian cell cycle. In contrast, homozygous deletion of Cdk1 causes early embryonic death in mice, because Cdk1-null embryos cannot undergo mitosis. Cdk1 is, therefore, the only Cdk essential for driving the mitotic cell cycle in mammals. In mammals, all oocytes are arrested at prophase of the first meiotic division when they are enclosed in individual ovarian follicles. Fully grown mouse oocytes resume meiosis as a result of a pre-ovulatory surge of luteinizing hormone (LH). This results in germinal vesicle (GV) breakdown (GVBD) followed by chromosome condensation, spindle formation and the completion of the first meiotic division. The resumption of meiosis in oocytes is often compared with the G 2 -M transition of mitosis, and the results from biochemical studies of mitosis are generalized to meiosis. Because Cdk1-null mice are not viable and all of the oocytes from Cdk2null mice are eliminated very early during meiosis, it remained unknown whether it is Cdk1 or Cdk2 that is essential for the resumption of meiosis in oocytes. Recent in vivo evidence has shown that Cdk1 is the only Cdk that is both Cdk1 drives meiosis and mitosis through two different mechanisms