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Vol. 14, Issue 1, 288-301, January 2003

Cell Cycle-dependent Regulation of Structure of Endoplasmic Reticulum and Inositol 1,4,5-Trisphosphate-induced Ca²⁺ Release in Mouse Oocytes and Embryos

Greg FitzHarris,^* Petros Marangos, and John Carroll

 Departments of Physiology and  ^*Obstetrics and Gynaecology and the Assisted Conception Unit, University College London, London, WC1E 6BT

The organization of endoplasmic reticulum (ER) was examined in mouse eggs undergoing fertilization and in embryos during the first cell cycle. The ER in meiosis II (MII)-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 by using the proteasome inhibitor MG132, or by microinjecting excess 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. Inositol 1,4,5-trisphosphate-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 inositol 1,4,5-trisphosphate-induced Ca²⁺ release have implications for understanding meiotic and mitotic control of ER structure and inheritance, and of the mechanisms regulating mitotic Ca²⁺ signaling.

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Corresponding author. E-mail address: j.carroll{at}ucl.ac.uk.

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Molecular Biology of the Cell
Vol. 14, 288-301, January 2003
Copyright © 2003 by The American Society for Cell Biology

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