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Reproduction (2008) 136 741-752
DOI: 10.1530/REP-08-0271
Copyright © 2008 Society for Reproduction and Fertility
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RESEARCH

Fertilization differently affects the levels of cyclin B1 and M-phase promoting factor activity in maturing and metaphase II mouse oocytes

Anna Ajduk1,4, Maria A Ciemerych1,2, Victoria Nixon3, Karl Swann4 and Marek Maleszewski1

Departments of1 , Embryology2 Cytology, Institute of Zoology, University of Warsaw, Miecznikowa 1, 02-096 Warsaw, Poland3 Department of Anatomy and Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK4 Department of Obstetrics and Gynaecology, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK

Correspondence should be addressed to A Ajduk; Email: aajduk{at}biol.uw.edu.pl

Fertilization affects levels of cyclin B1 and M-phase promoting factor (MPF) activity in maturing and metaphase II mouse oocytes in two distinct ways. In metaphase II oocytes, it leads to a Ca2+-dependent, continuous degradation of cyclin B1 and inactivation of cyclin dependent kinase (CDC2A)–cyclin B1 complex (MPF). In this paper, we show that neither mono- nor polyspermic fertilization of prometaphase I and metaphase I oocytes triggered degradation of cyclin B1. However, polyspermic fertilization of prometaphase I oocytes led to a transient decrease in MPF activity that lasted for 2 h. The inactivation of MPF in polyspermic prometaphase I oocytes did not depend on the fertilization-induced increase in the cytoplasmic concentration of free Ca2+ ions, but was caused, at least in part, by dephosphorylation of CDC2A at threonine 161 (Thr161). We found that polyspermic fertilization did not affect glutathione levels in prometaphase I oocytes, and concluded that the decrease in MPF activity and dephosphorylation of CDC2A at Thr161 in polyspermic prometaphase I oocytes were not caused by a change in the redox status of the cell induced by an introduction of excessive amount of sperm protamines. Instead, we propose that inactivation of MPF activity in polyspermic maturing oocytes is caused by a change in nucleo-cytoplasmic ratio that leads to a ‘titration’ of kinases and phosphatases responsible for keeping MPF in an active state. This idea is supported by the finding that oocytes fused with thymocytes rather than spermatozoa also showed a transient decrease in MPF activity.







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