| First Author | Lefèvre B | Year | 2007 |
| Journal | Crit Rev Eukaryot Gene Expr | Volume | 17 |
| Issue | 4 | Pages | 259-69 |
| PubMed ID | 17725492 | Mgi Jnum | J:169990 |
| Mgi Id | MGI:4943666 | Doi | 10.1615/critreveukargeneexpr.v17.i4.10 |
| Citation | Lefevre B, et al. (2007) The phosphoinositide-phospholipase C (PI-PLC) pathway in the mouse oocyte. Crit Rev Eukaryot Gene Expr 17(4):259-69 |
| abstractText | As highlighted in this review, the phosphoinositide-phospholipase C pathway is strongly implicated in the control of mouse oocyte meiosis. The pathway becomes progressively functional as oocyte growth advances, and it appears to play a role in the G2/M transition when meiosis resumes, at least in the in vitro spontaneous model. Even if the inositol 1,4,5-trisphosphate receptors are present from the beginning, they function and release Ca2+ when the follicular antrum appears. Phospholipase C beta1 (PLC beta 1) is first exclusively localized to the nucleus and then migrates to the cytoplasm when the oocyte is fully grown. During oocyte maturation PLC beta 1 is active in the cytoplasm before it migrates and becomes active in the nucleus just prior to germinal vesicle breakdown. Because a similar circuit is observed for protein kinase C alpha (PKC alpha), PKC beta 1, PKC beta 2, and active mitogen-activated protein kinase, it is tempting to envisage that a feedback loop occurs between these pathways as demonstrated in other cell types. The chronology of these molecular movements into the oocyte reveals the particular and important role of the nucleus phosphoinositide cycle during oocyte meiosis. It appears also that this chronology is crucial and that defects leading to an inappropriate intracellular localization can have dramatic consequences. Such anomalies can prevent the production of competent oocytes and lead to fertility problems. |
