Abstract
Mutations in cortex and grauzone cause abnormal arrest in Drosophila female meiosis. cortex was mapped to a 14 kb interval in 26F-27A by the male recombination mapping method. While these experiments mapped the gene accurately, they also illustrated some complexities of this method. Rescue results showed that a 2.8 kb genomic fragment from this interval was able to fully rescue the cortex phenotype. The 2.8 kb rescuing fragment contains a single open reading frame. The predicted amino acid sequence indicates that cortex encodes a WD-repeat protein and is a distant member of the Cdc20 protein family. Results from a developmental Northern analysis showed that the cortex transcript is expressed at high levels during oogenesis and early embryogenesis. Interestingly, the meiotic metaphase-anaphase II arrest defect in embryos laid by cortex homozygous females resembles the mitotic metaphase-anaphase defects observed in yeast cdc20 mutants. The predicted nature of the Cortex protein, together with the observed meiotic phenotype in cortex mutants, suggest that a similar pathway to the cdc20 dependent APC-mediated proteolysis pathway, which governs the metaphase-anaphase transition in mitosis, is also important in regulating oocyte meiosis.
