During mammalian fertilization, the sperm induces oscillatory changes in the egg’s intracellular concentration of free calcium ([Ca2+]i) that are essential for initiating egg activation and subsequent embryo development. The mechanism(s) by which fertilization-associated [Ca2+]i oscillations are initiated remains elusive but may involve the activation of the phosphoinositide (PI) pathway. Stimulation of this pathway causes activation of a phospholipase C (PLC) isoform that, in turn, mediates the production of inositol 1,4,5-triphosphate (IP3). IP3 then induces Ca2+ release from the endoplasmic reticulum (ER).
In echinoderm and Xenopus eggs, increased turnover of PI lipids and IP3 production have been detected around the time of fertilization, although not in single cells, whereas in mammalian eggs determination of IP3 production during fertilization has not been possible because of fertilization asyn-chrony and the small size of the eggs.
Two mechanisms have been hypothesized by which the sperm may initiate the signaling cascade that culminates in [Ca2+]i oscillations. One hypothesis is that the sperm acts on an egg plasma membrane receptor, suggested to be a G-protein or a tyrosine kinase-coupled receptor, which upon sperm binding activates the PI pathway, leading to Ca2+ release.