| First Author | Wakai T | Year | 2013 |
| Journal | J Cell Sci | Volume | 126 |
| Issue | Pt 24 | Pages | 5714-24 |
| PubMed ID | 24101727 | Mgi Jnum | J:211535 |
| Mgi Id | MGI:5575625 | Doi | 10.1242/jcs.136549 |
| Citation | Wakai T, et al. (2013) Regulation of endoplasmic reticulum Ca(2+) oscillations in mammalian eggs. J Cell Sci 126(Pt 24):5714-24 |
| abstractText | Changes in the intracellular concentration of free calcium ([Ca(2+)]i) regulate diverse cellular processes including fertilization. In mammalian eggs, the [Ca(2+)]i changes induced by the sperm unfold in a pattern of periodical rises, also known as [Ca(2+)]i oscillations. The source of Ca(2+) during oscillations is the endoplasmic reticulum ([Ca(2+)]ER), but it is presently unknown how [Ca(2+)]ER is regulated. Here, we show using mouse eggs that [Ca(2+)]i oscillations induced by a variety of agonists, including PLCzeta, SrCl2 and thimerosal, provoke simultaneous but opposite changes in [Ca(2+)]ER and cause differential effects on the refilling and overall load of [Ca(2+)]ER. We also found that Ca(2+) influx is required to refill [Ca(2+)]ER, because the loss of [Ca(2+)]ER was accelerated in medium devoid of Ca(2+). Pharmacological inactivation of the function of the mitochondria and of the Ca(2+)-ATPase pumps PMCA and SERCA altered the pattern of oscillations and abruptly reduced [Ca(2+)]ER, especially after inactivation of mitochondria and SERCA functions. We also examined the expression of SERCA2b protein and found that it was expressed throughout oocyte maturation and attained a conspicuous cortical cluster organization in mature eggs. We show that its overexpression reduces the duration of inositol-1,4,5-trisphosphate-induced [Ca(2+)]i rises, promotes initiation of oscillations and enhances refilling of [Ca(2+)]ER. Collectively, our results provide novel insights on the regulation of [Ca(2+)]ER oscillations, which underlie the unique Ca(2+)-signalling system that activates the developmental program in mammalian eggs. |
