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In mammalian cells, cyclin B1 plays a pivotal role in mitotic and meiotic progression. It has been reported that infertility occurs after disruption of  cyclin B1  ( Ccnb1 ) in male germ cells and oocytes. However, it remains to be elucidated whether the specific disruption of  Ccnb1  in granulosa cells influences the reproductive activity of female mice. Amhr2 is expressed in granulosa cells (GCs) of the ovary. Here, we mated  Ccnb1 Flox/Floxmice with a transgenic mouse strain expressing  Amhr2-Cre  to generate GC-specific  Ccnb1  knockout mice. The results showed that  Ccnb1  Flox/Flox , Amhr2-Cre  ( Ccnb1  cKO) mice were subfertile but had normal oocyte meiotic progress, spindle shape and protein levels of cohesin subunits REC8 and SMC3 on arm chromosomes during meiosis I. A further study found that 32.4% of oocytes from  Ccnb1  cKO mice exhibited chromosome condensation and spindle disassembly after the first polar body extrusion and failed to undergo second meiosis, which was never found in oocytes from  Ccnb1 Flox/Floxmice. In addition, the percentages of 2-cell embryos, morulas, and blastocysts in the  Ccnb1  mutant group were all dramatically decreased compared to those in the  Ccnb1 Flox/Floxgroup (39.2%  vs . 86.8%, 26.0%  vs . 85.0%, 19.1%  vs . 85.8%, respectively). Therefore, GC-specific  Ccnb1  deletion in mice could cause fewer and poor-quality blastocysts and subsequent subfertility, which plays an important role in understanding the function of cyclin B1 in reproduction.

Knockout of cyclin B1 in granulosa cells causes female subfertility