Reproduction Abstracts

Cyclin A, the first cyclin ever cloned, is thought to be an essential component of the cell-cycle engine. Mammalian cells encode two A-type cyclins, a testis-specific cyclin A1 and a ubiquitously expressed cyclin A2. Cyclin A2 is an essential mitotic CDK regulatory partner and is attributed with a wide range of effects early in the G2–M transition. Although its role in mitosis has been extensively investigated, research into the role of cyclin A2 in meiosis is lacking. In order to investigate the functions of cyclin A2 in meiosis we have developed two models: the cyclin A2 overexpression model with GFP-tagged cyclin A2 protein microinjection and conditional knockout model with created cyclin A2^f/f; Zp3 Cre mouse. With the GFP-tagged cyclin A2 protein microinjection in the GV stage mouse oocytes, and together with live cell imaging indicate the subcellular localization of cyclin A2. The conditional knockout mice were created by crossing cyclin A2 floxed mice with the Zp3 Cre mice. With the microinjection of the cyclin A2–GFP protein, we found that the overexpression of cyclin A2 could delay the MI–AI stage transition. The fertility experiment and superovulation experiment with the cyclin A2^f/f; Zp3 Cre mice indicated that the depletion of cyclin A2 could cause the aneuploidy during the first polar body extrusion and finally reduce the infertility of the mice. In conclusion, we have found that cyclin A2 is necessary to create a cellular environment that ensures normal oocyte growth and the faithful segregation of the chromosomes.