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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Vol. 78 • No. 4