Journal
BIOLOGY OF REPRODUCTION
Volume 78, Issue 4, Pages 726-735Publisher
OXFORD UNIV PRESS INC
DOI: 10.1095/biolreprod.107.063693
Keywords
aurora kinase A; calcium; gamete biology; meiosis; oocyte development
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Funding
- NCRR NIH HHS [RR20146, P20 RR020146] Funding Source: Medline
- NIA NIH HHS [R01 AG013081, AG13081] Funding Source: Medline
- NICHD NIH HHS [R01 HD035688-08A2, R01 HD035688, HD35688] Funding Source: Medline
- NIGMS NIH HHS [R01 GM061829, R01 GM061829-08, R01 GM061829-07, GM-61829] Funding Source: Medline
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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.
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