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.
Highlights
The studies of gamete maturation and fertilization have been intimately associated with the regulation of ionic currents in these cells
Even when the T-type current is prominent in mouse eggs, mice null for this channel, Cacna1h−/− (Chen et al, 2003), showed only marginal subfertility (Bernhardt et al, 2015). These results suggest that the function of this channel may be to support Ca2+ influx during the germinal vesicle arrest (GV; Figure 1) and during maturation
The scientific evidence shows that for mammalian eggs, the blockade of polyspermy must be a combination of mechanisms, including changes in the membrane potential, reorganization of proteins expressed at the plasma membrane (PM) and even intracellular re-arrangements (Bianchi and Wright, 2016)
Summary
Acquiring fertilization competence requires resumption of meiosis which encompasses the remodeling of multiple signaling pathways and the reorganization of cellular organelles This differentiation endows the egg with the ability to activate at fertilization and to promote the egg-to-embryo transition. 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.
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