Meiosis and early cleavage in Drosophila melanogaster eggs: effects of the claret-non-disjunctional mutation.

The claret-non-disjunctional (cand) mutation is a female-specific mutation in Drosophila melanogaster, which causes a high frequency of mortality (89--90%) in eggs laid by the homozygous females. Among the progeny that survive to the adult stage, greater than 50% are aneuploid and/or mosaic for the X and number 4 chromosomes. The genetic studies of cand indicate that it is homologous to the claret mutation (ca-simulans) in Drosophila simulans. The cytological effect of the cand mutation on meiosis I and the early cleavage divisions has been observed at the light microscope level in stage 14 ovarian and fertilized uterine eggs, respectively. Four classes of metaphase I figures were observed. These include those with: (1) two or more spindles; (2) spindles that were abnormally wide and the bivalents widely separated; (3) unipolar spindles; and (4) apparently normal bipolar spindles. The three abnormal classes of metaphase I figures included 80% of the eggs examined at this stage. Among the cleavage stage eggs examined 69% showed highly abnormal mitotic figures, including multipolar spindles, and the nuclei in these eggs were found in clusters, rather than dispersed throughout the ooplasm. In addition to the cytological abnormalities observed, 17--23% of the eggs produced by the cand females showed morphological abnormalities. These abnormalities included eggs having three of four dorsal filaments, eggs that had a truncated shape, and abnormally small eggs. These abnormalities may not be an aspect of the cand syndrome, but they are due to recessive genes located on the third chromosome. Although the cand and ca-simulans mutations both affect the formation of the spindle apparatus during meiosis and the early cleavage divisions, the effects of these two mutations differ considerably in detail. The effect of the ca-simulans mutation appears to be more severe than the effect of cand. A model to explain the relationship between the effect of the cand mutation on meiosis I and the early cleavage divisions is presented, and evidence to support the model is discussed.