Abstract
Calcium (Ca2+) signals initiate egg activation across the animal kingdom and in at least some plants. These signals are crucial for the success of development and, in the case of mammals, health of the offspring. The mechanisms associated with fertilization that trigger these signals and the molecules that regulate their characteristic patterns vary widely. With few exceptions, a major contributor to fertilization-induced elevation in cytoplasmic Ca2+ is release from endoplasmic reticulum stores through the IP3 receptor. In some cases, Ca2+ influx from the extracellular space and/or release from alternative intracellular stores contribute to the rise in cytoplasmic Ca2+. Following the Ca2+ rise, the reuptake of Ca2+ into intracellular stores or efflux of Ca2+ out of the egg drive the return of cytoplasmic Ca2+ back to baseline levels. The molecular mediators of these Ca2+ fluxes in different organisms include Ca2+ release channels, uptake channels, exchangers and pumps. The functions of these mediators are regulated by their particular activating mechanisms but also by alterations in their expression and spatial organization. We discuss here the molecular basis for modulation of Ca2+ signalling at fertilization, highlighting differences across several animal phyla, and we mention key areas where questions remain.
Highlights
How the terminally differentiated gametes interact with each other at fertilization to initiate the development of a new organism is a question that has fascinated scientists for over a century
Fertilizationinduced Ca2+ changes depend on a large number of variables including exactly how the Ca2+ rise is initiated and how the newly formed zygote responds to this Ca2+ rise and perhaps to other signalling pathways triggered at fertilization
Overexpression in eggs of a phosphomimetic IP3R1 protein in which the two cyclin-dependent kinase 1 (CDK1) consensus sites (S421 and T799) and the ERK consensus site (S436) were mutated to aspartic acid led to increased sensitivity of the receptor to PLCζ injection or caged IP3 expression [39]. These findings strongly suggest that CDK1and mitogen-activated protein kinase (MAPK)-mediated phosphorylation of IP3R1 explains at least part of the increase in IP3 sensitivity that occurs during maturation
Summary
How the terminally differentiated gametes interact with each other at fertilization to initiate the development of a new organism is a question that has fascinated scientists for over a century. Golgi membranes contain functional IP3 receptors [56], but the possible contributions of this organelle to Ca2+ release during egg activation is unknown It is unclear if there is an important role for the reorganization of the Golgi apparatus during oocyte maturation, or whether it is a response to major ER rearrangements or changing trafficking demands. Biochemical studies in sea urchins documented a rapid rise in both triphosphoinositides and diphosphoinositides that occurred after insemination but prior to evidence of Ca2+ release, suggesting that IP3 mediates Ca2+ release as had been shown previously in somatic cells [93] This idea was tested by microinjection of IP3 into sea urchin eggs, which resulted in exocytosis of cortical granules and elevation of the fertilization envelope, both indicators of an increase in cytoplasmic Ca2+ concentration [94].
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