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A more recent version of this article appeared on January 1, 2003
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Submitted on July 26, 2002
Revised on September 17, 2002
Accepted on October 3, 2002
1 Department of Physiology, Department of Obstetrics and Gynaecology and the Assisted Conception Unit, University College London, University College London, Gower Street, London, WC1E 6BT
2 Department of Physiology, University College London, Gower Street, London, WC1E 6BT
* Corresponding author. E-mail address: j.carroll{at}ucl.ac.uk.
The organization of endoplasmic reticulum was examined in mouse eggs undergoing fertilization and in embryos during the first cell cycle. The ER in meiosis II-arrested mouse eggs is characterized by accumulations (clusters) that are restricted to the cortex of the vegetal hemisphere of the egg. Monitoring ER structure with DiI18 after egg activation has demonstrated that ER clusters disappear at the completion of meiosis II. The ER clusters can be maintained by inhibiting the decrease in cdk1-cyclin B activity using the proteasome inhibitor, MG132, or by microinjecting excess GFP-cyclin B. A role for cdk1-cyclin B in ER organization is further suggested by the finding that the cdk inhibitor, roscovitine, causes the loss of ER clusters in MII eggs. Cortical clusters are specific to meiosis as they do not return in the first mitotic division, rather, the ER aggregates around the mitotic spindle. InsP3-induced Ca2+ release is also regulated in a cell cycle dependent manner where it is increased in MII and in the first mitosis. The cell cycle dependent effects on ER structure and InsP3-induced Ca2+ release have implications for understanding meiotic and mitotic control of ER structure and inheritance, and of the mechanisms regulating mitotic Ca2+ signalling.
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