| First Author | Zhang Y | Year | 2019 |
| Journal | J Cell Physiol | Volume | 234 |
| Issue | 10 | Pages | 18513-18523 |
| PubMed ID | 30912144 | Mgi Jnum | J:290769 |
| Mgi Id | MGI:6442753 | Doi | 10.1002/jcp.28487 |
| Citation | Zhang Y, et al. (2019) Loss of PKC mu function induces cytoskeletal defects in mouse oocyte meiosis. J Cell Physiol 234(10):18513-18523 |
| abstractText | Cytoskeleton which includes microtubule and actin filaments plays important roles during mammalian oocyte maturation. In the present study, we showed that protein kinase C mu (PKC mu) was one potential key molecule which affected cytoskeleton dynamics in mouse oocytes. Our results showed that PKC mu expressed and localized at the poles of the spindle during oocyte maturation, and PKC mu expression reduced in the oocytes from 6-month-old mice or 24 hr in vitro culture. We knocked down the expression of PKC mu in oocytes using morpholino injection to explore the relationship between PKC mu and subcellular structure defects. The loss of PKC mu reduced oocyte maturation competence, showing with decreased polar body extrusion rate and increased rate of symmetric division. Further analysis indicated that PKC mu decrease caused the spindle organization defects, and this could be confirmed by the decreased tubulin acetylation level. Moreover, we found that PKC mu affected the phosphorylation level of cofilin for actin assembly, which further affected cytoplasmic actin distribution and spindle positioning. In summary, our data indicated that PKC mu is one key factor for oocyte maturation through its roles on the spindle organization and actin filament distribution. |
