| First Author | Wakai T | Year | 2019 |
| Journal | J Cell Sci | Volume | 132 |
| Issue | 3 | PubMed ID | 30659110 |
| Mgi Jnum | J:272330 | Mgi Id | MGI:6280631 |
| Doi | 10.1242/jcs.225441 | Citation | Wakai T, et al. (2019) Constitutive IP3R1-mediated Ca(2+) release reduces Ca(2+) store content and stimulates mitochondrial metabolism in mouse GV oocytes. J Cell Sci 132(3):jcs225441 |
| abstractText | In mammals, fertilization initiates Ca(2+) oscillations in metaphase II oocytes, which are required for the activation of embryo development. Germinal vesicle (GV) oocytes also display Ca(2+) oscillations, although these unfold spontaneously in the absence of any known agonist(s) and their function remains unclear. We found that the main intracellular store of Ca(2+) in GV oocytes, the endoplasmic reticulum ([Ca(2+)]ER), constitutively 'leaks' Ca(2+) through the type 1 inositol 1,4,5-trisphosphate receptor. The [Ca(2+)]ER leak ceases around the resumption of meiosis, the GV breakdown (GVBD) stage, which coincides with the first noticeable accumulation of Ca(2+) in the stores. It also concurs with downregulation of the Ca(2+) influx and termination of the oscillations, which seemed underpinned by the inactivation of the putative plasma membrane Ca(2+) channels. Lastly, we demonstrate that mitochondria take up Ca(2+) during the Ca(2+) oscillations, mounting their own oscillations that stimulate the mitochondrial redox state and increase the ATP levels of GV oocytes. These distinct features of Ca(2+) homeostasis in GV oocytes are likely to underpin the acquisition of both maturation and developmental competence, as well as fulfill stage-specific cellular functions during oocyte maturation. |
