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Reproduction (2004) 127 455-463
DOI: 10.1530/rep.1.00104
Copyright © 2004 Society for Reproduction and Fertility
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RESEARCH

Are Src family kinases involved in cell cycle resumption in rat eggs?

A Talmor-Cohen, R Tomashov-Matar, E Eliyahu, R Shapiro and R Shalgi

Department of Cell and Developmental Biology, Sackler Faculty of Medicine, Tel Aviv University, Ramat-Aviv 69978, Tel-Aviv, Israel

Correspondence should be addressed to R Shalgi; Email: shalgir{at}post.tau.ac.il

The earliest visible indications for the transition to embryos in mammalian eggs, known as egg activation, are cortical granules exocytosis (CGE) and resumption of meiosis (RM); these events are triggered by the fertilizing spermatozoon through a series of Ca2+ transients. The pathways, within the egg, leading to the intracellular Ca2+ release and to the downstream cellular events, are currently under intensive investigation. The involvement of Src family kinases (SFKs) in Ca2+ release at fertilization is well supported in marine invertebrate eggs but not in mammalian eggs. In a previous study we have shown the expression and localization of Fyn, the first SFK member demonstrated in the mammalian egg. The purpose of the current study was to identify other common SFKs and resolve their function during activation of mammalian eggs. All three kinases examined: Fyn, c-Src and c-Yes are distributed throughout the egg cytoplasm. However, Fyn and c-Yes tend to concentrate at the egg cortex, though only Fyn is localized to the spindle as well. The different localizations of the various SFKs imply the possibility of their different functions within the egg. To examine whether SFKs participate in the signal transduction pathways during egg activation, we employed selective inhibitors of the SFKs activity ((PP2 and SU6656). The results demonstrate that RM, which is triggered by Ca2+ elevation, is an SFK-dependent process, while CGE, triggered by either Ca2+ elevation or protein kinase C (PKC), is not. The possible involvement of SFKs in the signal transduction pathways that lead from the sperm–egg fusion site downstream of the Ca2+ release remains unclear.




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