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Fig. 7. Cks30A and Cortex mediate Cyclin A destruction. (A) Western blot from Cks30A^KO/Cks30A^KO and unfertilized wild-type embryos (0-2 hours after egg-laying) and ovaries probed for Cyclin A, B and B3, revealing excess Cyclin A in Cks30A mutants. The upper (active) form is particularly enriched. Far lane, Cks30A^KO extract at 1/12 dilution contains approximately equal Cyclin A concentrations to wild type (see Materials and methods), indicating a 12-fold excess of Cyclin A in the mutant. (B) RT-PCR on wild-type and Cks30A^KO/Cks30A^KO ovaries and embryos (0-2 hours after egg-laying) reveals similar cyclin A mRNA concentrations. (C) Embryo from Cks30A^RA74/Cks30A^KO;cycA^C8LR1/+ female (0-2 hours after egg-laying). Reduction of cyclin A dosage partially suppresses the Cks30A mutant phenotype, allowing some embryos to develop normally through several syncytial divisions. Mitotic spindles in this embryo are bipolar and are evenly spaced (compare to Fig. 1C – both embryos are at a similar stage, with approximately 32 nuclei). (D) Western blot from wild-type and cort^QW55 ovaries probed for Cyclin A and B reveals an elevated concentration of Cyclin A. (E) Northern blot from wild-type and Cks30A^HG24/Cks30A^HG24 ovaries probed for fzy and cortex mRNA shows equal transcript concentrations, and (below) western blot from wild-type and Cks30A^KO/Cks30A^KO ovaries probed for Fzr protein, showing wild-type concentrations of Fzr protein. The upper band is non-specific and serves as a loading control.

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