Lack of protein kinase C‐delta (PKCδ) disrupts fertilization and embryonic development

SUMMARY This study tested the function of protein kinase C delta (PKCδ) during fertilization and embryonic development using gene‐knockout ( Prkcd −/− ) mice. Fertility analysis revealed that Prkcd −/− mating pairs produce significantly fewer pups per litter than wild‐type pairs ( P  < 0.05), and exhibit a high incidence of embryonic loss post‐implantation. Both Prkcd −/− male as well as Prkcd −/− female mice mated to Prkcd +/+ controls also showed reduced litter sizes, with a selective loss of Prkcd ‐null pups. Further analysis of the females demonstrated comparable in vitro fertilization outcomes between control and Prkcd −/− oocytes fertilized with wild‐type sperm. Pregnant Prkcd −/− females, however, exhibited a reduced number of total implantations, suggesting a possible disruption in early embryo quality and/or implantation. In turn, male gamete analysis revealed that Prkcd −/− sperm demonstrated a decreased capacity to penetrate the zona pellucida ( P  < 0.05), necessary for successful fertilization. Moreover, we identified phosphorylated PKCδ as a component of the sperm acrosome, indicating a potential role for this kinase in acrosome exocytosis. Therefore, loss of PKCδ disrupts key reproductive functions in both males and females that limit fertility. Mol. Reprod. Dev. 82: 797–808, 2015. © 2015 Wiley Periodicals, Inc .