In Drosophila, normal female meiosis arrests at metaphase I. After meiotic arrest is released by egg activation, the two meiotic divisions are rapidly completed, even in unfertilized eggs. Since little is known about the regulation of the meiotic cell cycle after the meiotic arrest, we screened for mutants that arrest in meiosis. Here we describe the phenotype of eggs laid by sterile mothers mutant for either grauzone or cortex. These eggs arrest in metaphase of meiosis II, and although they can enter into an aberrant anaphase II, they never exit meiosis. Prolonged sister-chromatid cohesion is not the cause of this arrest, since a premature release of sister cohesion does not rescue the meiotic arrest of cortex eggs. Aberrant chromosome segregation at meiosis I was the earliest observable defect, suggesting that grauzone and cortex are first required immediately after egg activation. The cortical microtubules are also defective, remaining in a pre-activated state in activated mutant eggs. The mutations had no observable effect on either male meiosis or mitosis. We believe these genes will provide insight into the developmental regulation of meiosis in a genetically tractable organism.