Only a minority of spindles in non-activated Cks30A^RA74 oocytes show normal spindle morphology and chromosome alignment. Approximately half of the spindles show chromosome misalignment; chiasmatic chromosomes often move away from the equator and lose overall symmetrical distribution. Abnormal spindle morphology is also seen, with the most typical defect being the formation of ectopic poles near the spindle equator. The spindles are longer in the mutants (21.1 +/- 5.7 μm) than in controls (14.7 +/- 5.8 μm).

Embryos derived from females homozygous or hemizygous for Cks30A^RA74 arrest development at the onset of embryogenesis, typically with a single metaphase mitotic spindle. Some embryos progress through a limited number of divisions before arresting, again in a metaphase-like state. These metaphase-arrested spindles are zygotic and not derived from the female meiotic spindle. In Cks30A^RA74 mutants, the first events of female meiosis are unaffected. The karyosome appears normal, and the timing of nuclear envelope breakdown and the appearance of the spindle is also unaffected in the majority of mutant ovaries, although approximately 7% have abnormal spindles and fail chromosome congression on the spindle. Consistent meiotic defects were detected upon ovulation and entry into the second meiotic division. Rotation of the spindle fails in the majority of oocytes, and assembly of the meiosis II spindle is abnormal. The most common defect in Cks30A^RA74 mutants is a kink and/or separation of the two tandem spindles. In more severe cases, the meiotic spindle breaks down and chromosome segregation is severely disrupted. Despite these errors, the female meiotic products appear to exit meiosis, reforming nuclear envelopes, and pronuclear fusion occurs. After completion of meiosis, the polar body microtubule aster does not form in Cks30A^RA74 mutants, instead a shell of microtubules surrounds the chromatin. Cks30A^RA74 and Cks30A^RA74/Cks30A^HG24 mutants exhibit defects in abdominal cuticle deposition, indicative of a partial disruption of larval abdominal histoblast development.

Eggs laid by females homozygous for Cks30A^RA74 show no visible sign of development when observed under transmitted light in stereomicroscope.

Eggs derived from homozygous females show no visible sign of embryonic development when observed under transmitted light in a stereo microscope. After 4-6 hours after egg deposition the originally unformly dense (like wild type) yolk mass starts to disintegrate into a network of darker and lighter yolk droplets. The defect may be in fertilisation or very early in embryonic development.