| First Author | Ma W | Year | 2015 |
| Journal | Mol Reprod Dev | Volume | 82 |
| Issue | 10 | Pages | 797-808 |
| PubMed ID | 26202826 | Mgi Jnum | J:325872 |
| Mgi Id | MGI:6875247 | Doi | 10.1002/mrd.22528 |
| Citation | Ma W, et al. (2015) Lack of protein kinase C-delta (PKCdelta) disrupts fertilization and embryonic development. Mol Reprod Dev 82(10):797-808 |
| abstractText | This study tested the function of protein kinase C delta (PKCdelta) 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 PKCdelta as a component of the sperm acrosome, indicating a potential role for this kinase in acrosome exocytosis. Therefore, loss of PKCdelta disrupts key reproductive functions in both males and females that limit fertility. |
