Induction of Maturation-Promoting Factor during Xenopus oocyte Maturation Uncouples Ca2+ Store Depletion from Store-Operated Ca2+ Entry

During oocyte maturation, eggs acquire the ability to generate specialized Ca2+ signals in response to sperm entry. Such Ca2+ signals are crucial for egg activation and the initiation of embryonic development. We examined the regulation during Xenopus oocyte maturation of store-operated Ca2+ entry (...

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Bibliographic Details
Published in:The Journal of cell biology 2002-01, Vol.156 (1), p.75-85
Main Authors: Machaca, Khaled, Haun, Shirley
Format: Article
Language:English
Subjects:
Calcium
Cell division
Cells
Cyclins
Eggs
Embryos
Enzymes
Fertilization
Ions
Meiosis
Oocytes
Ova
Reproduction
RNA
T lymphocytes
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Summary:During oocyte maturation, eggs acquire the ability to generate specialized Ca2+ signals in response to sperm entry. Such Ca2+ signals are crucial for egg activation and the initiation of embryonic development. We examined the regulation during Xenopus oocyte maturation of store-operated Ca2+ entry (SOCE), an important Ca2+ influx pathway in oocytes and other nonexcitable cells. We have previously shown that SOCE inactivates during Xenopus oocyte meiosis. SOCE inactivation may be important in preventing premature egg activation. In this study, we investigated the correlation between SOCE inactivation and the Mos-mitogen-activated protein kinase (MAPK)-maturation-promoting factor (MPF) kinase cascade, which drives Xenopus oocyte maturation. SOCE inactivation at germinal vesicle breakdown coincides with an increase in the levels of MAPK and MPF. By differentially inducing Mos, MAPK, and MPF, we demonstrate that the activation of MPF is necessary for SOCE inactivation during oocyte maturation. In contrast, sustained high levels of Mos kinase and the MAPK cascade have no effect on SOCE activation. We further show that preactivated SOCE is not inactivated by MPF, suggesting that MPF does not block Ca2+ influx through SOCE channels, but rather inhibits coupling between store depletion and SOCE activation.
ISSN:0021-9525
1540-8140
DOI:10.1083/jcb.200110059