The involvement of Src family kinases (SFKs) in the events leading to resumption of meiosis

Abstract

Ovulated mammalian eggs remain arrested at the second meiotic metaphase (MII) until fertilization. The fertilizing spermatozoon initiates a sequence of biochemical events, collectively referred to as ‘egg activation’, which overcome this arrest. The initial observable change within the activated egg is a transient rise in intracellular Ca 2+ concentration ([Ca 2+] i) followed by cortical granule exocytosis (CGE) and resumption of the second meiotic division (RMII). To date, the mechanism by which the fertilizing spermatozoon activates the signaling pathways upstream to the Ca 2+ release and the manner by which the signals downstream to Ca 2+ release evoke RMII are not well documented. Protein tyrosine kinases (PTKs) were suggested as possible inducers of some aspects of egg activation. Src family kinases (SFKs) constitute a large family of evolutionarily conserved PTKs that mediate crucial biological functions. At present, the theory that one or more SFKs are necessary and sufficient for Ca 2+ regulation at fertilization is documented in eggs of marine invertebrates. The mechanism leading to Ca 2+ release during fertilization is less established in mammalian eggs. A controversy still exists as to whether SFKs within the mammalian egg are sufficient and/or necessary for Ca 2+ release, or whether they play a role during egg activation via other signaling pathways. This article summarizes the possible signaling pathways involved upstream to Ca 2+ release but focuses mainly on the involvement of SFKs downstream to Ca 2+ release toward RMII, in invertebrate and vertebrate eggs.