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.