Ion Channel Function During Oocyte Maturation and Fertilization

Abstract

The proper maturation of both male and female gametes is essential for supporting fertilization and the early embryonic divisions. In the ovary, immature fully-grown oocytes that are arrested in prophase I of meiosis I are not able to support fertilization. Acquiring fertilization competence requires resumption of meiosis which encompasses the remodeling of multiple signaling pathways and the reorganization of cellular organelles. Collectively, this differentiation endows the egg with the ability to activate at fertilization and to promote the egg-to-embryo transition. Oocyte maturation is associated with changes in the electrical properties of the plasma membrane and alterations in the function and distribution of ion channels. Therefore, variations on the pattern of expression, distribution, and function of ion channels and transporters during oocyte maturation are fundamental to reproductive success. Ion channels and transporters are important in regulating membrane potential, but also in the case of calcium (Ca2+), they play a critical role in modulating intracellular signaling pathways. In the context of fertilization, Ca2+ has been shown to be the universal activator of development at fertilization, playing a central role in early events associated with egg activation and the egg-to-embryo transition. These early events include the block of polyspermy, the completion of meiosis and the transition to the embryonic mitotic divisions. In this review, we discuss the role of ion channels during oocyte maturation, fertilization and early embryonic development. We will describe how ion channel studies in Xenopus oocytes, an extensively studied model of oocyte maturation, translate into a greater understanding of the role of ion channels in mammalian oocyte physiology.

Dynamics expression of DmFKBP12/Calstabin during embryonic early development of Drosophila melanogaster

“…As the crucial regulator of this CICR pathway along with binding protein of IP3R as well [47], in which four DmFKBP12 control opening of ER/SR DmRyR tetramer, the expression and function of DmFKBP12 should be carried out in the lava stage. Because of, as discussed above, RyR-mediated CICR exhibiting with calcium spark and calcium wave robusting from fertilization of many animals [48–51], it is judicious that the DmRyR-FKBP12 complex functions as early as the same stage. Our data in this investigation demonstrated that the DmFKBP12 distributed in subsurface cortex apposition to the plasma membrane in syncytial blastoderm (Figs.…”

Ca2+Signaling and Homeostasis in Mammalian Oocytes and Eggs

“…The mouse egg predominantly expresses an LVA VGC known as Ca V 3.2 (T-type) (Peres 1986;Kang et al 2007;Bernhardt et al 2015). Evidence suggests that the functional expression of these channels changes during maturation, as mouse GV oocytes display larger Ca V 3.2-mediated currents than MII eggs (Bernhardt et al 2015;Carvacho et al 2018), although the nature of these changes and mode of regulation remains to be well established. It is apparent, however, that mice null for the Ca V 3.2 gene, Cacna1h, only show mild subfertility and sperm-induced oscillations are largely unaffected (Bernhardt et al 2015).…”

Regulation of [Ca2+]i oscillations and mitochondrial activity by various calcium transporters in mouse oocytes

“…The importance of Ca 2+ functions in the regulation of oocyte activation is increasingly being recognized [6]. There are many important channel proteins involved in Ca 2+ transport in oocytes.…”