The synaptonemal complex assembles with proper timing and morphology in the ovaries of Cap-G^Z1/Cap-G^K4 females. However, there is a clear delay in disassembly of the synaptonemal complex in the mutant ovaries.

Stage 12 and 13 oocytes show a modest increase in the number of prometaphase I configurations with separated chromosomes in Cap-G^Z1/Cap-G^K4 females. Stage 14 oocytes show a dramatic increase in metaphase I defects, most commonly multiple chromosome masses. This phenotype is recessive. Premature sister chromatid separation is not seen, but the X homologs and autosomes do prematurely disjoin from their bivalents.

Embryos derived from Cap-G^Z1/Cap-G^K4 females arrest early, with defects such as polyploid masses.

Prophase and prometaphase chromosomes show a range in the level of chromosome condensation in dividing cells in postblastoderm Cap-G^K4/Df(2R)vg56 mutant embryos. This defect in the level of chromosome condensation is resolved by metaphase and the condensed chromosomes align appropriately on the mitotic spindle. At anaphase, sister chromatids fail to separate and only the fourth chromosomes separate and move to the spindle poles. Lagging chromatid arms are seen in telophase. Mutant postblastoderm embryos have an increased number of prometaphase figures compared to wild-type embryos, suggesting that the length of prometaphase may be increased in the mutant embryos. In dup^a1 Cap-G^K4 double mutants, cells at cycle 16 contain unreplicated chromosomes that fail to condense into discernible metaphase chromosomes.