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BOR - Papers in Press, published online ahead of print December 19, 2007.
Biol Reprod 2007, 10.1095/biolreprod.107.063693
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BIOLOGY OF REPRODUCTION 78, 726–735 (2008)
DOI: 10.1095/biolreprod.107.063693
© 2008 by the Society for the Study of Reproduction, Inc.

Ca2+ Homeostasis Regulates Xenopus Oocyte Maturation1

Lu Sun 3, Rawad Hodeify 3, Shirley Haun 3, Amanda Charlesworth 4, Angus M. MacNicol 3 4 7, Subramaniam Ponnappan 5, Usha Ponnappan 5 6 7, Claude Prigent 8, and Khaled Machaca 2 3 7

Departments of Physiology & Biophysics,3 Neurobiology & Developmental Sciences,4 Geriatrics5 and Immunology & Microbiology,6 and the Arkansas Cancer Research Center,7 University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205 CNRS UMR6061,8 Genetique et Developpement, Universite de Rennes 1, 35043 Rennes, France

ABSTRACT

In contrast to the well-defined role of Ca2+ signals during mitosis, the contribution of Ca2+ signaling to meiosis progression is controversial, despite several decades of investigating the role of Ca2+ and its effectors in vertebrate oocyte maturation. We have previously shown that during Xenopus oocyte maturation, Ca2+ signals are dispensable for entry into meiosis and for germinal vesicle breakdown. However, normal Ca2+ homeostasis is essential for completion of meiosis I and extrusion of the first polar body. In this study, we test the contribution of several downstream effectors in mediating the Ca2+ effects during oocyte maturation. We show that calmodulin and calcium-calmodulin-dependent protein kinase II (CAMK2) are not critical downstream Ca2+ effectors during meiotic maturation. In contrast, accumulation of Aurora kinase A (AURKA) protein is disrupted in cells deprived of Ca2+ signals. Since AURKA is required for bipolar spindle formation, failure to accumulate AURKA may contribute to the defective spindle phenotype following Ca2+ deprivation. These findings argue that Ca2+ homeostasis is important in establishing the oocyte's competence to undergo maturation in preparation for fertilization and embryonic development.

Aurora kinase A, calcium, gamete biology, meiosis, oocyte development


FOOTNOTES

1Supported by National Institutes of Health grants GM-61829 (K.M.), HD35688 (A.M.M.), AG13081 (U.P.), and RR20146 (A.C.). C.P. is funded by grants from the CNRS and LNCC (équipe labellisée).

Correspondence: 2Khaled Machaca, Department of Physiology & Biophysics, 4301 West Markham St., Slot 505, University of Arkansas for Medical Sciences (UAMS), Little Rock, AR 72205. FAX: 501 686 8167; e-mail: kamachaca{at}uams.edu.







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Copyright © 2008 by the Society for the Study of Reproduction.