In many animals female meiotic spindles lack centrosomes. In the absence of centrosomes the chromosomes drive spindle formation. This process is not well understood so I examined two mutants from a screen for female sterile mutations with acentrosomal spindle defects. I found that the first mutant, remnants (rem), disrupted spindle morphology, chromosome alignment and microtubule dynamics in non-activated oocytes. rem encodes Cks30A a conserved subunit of Cdc2. Essential pole proteins, msps and D-TACC were often mislocalised to the equator and Cks30A is involved in modification of D-TACC. The second mutant, msps-like, had tripolar spindles in non-activated oocytes. I found that msps-like encodes Weel, a negative regulator of Cdc2 activity. Wee1 is also required for modification of D-TACC in a Cdc2 dependent manner. Twine, the positive regulator of Cdc2, is essential for spindle unification/metaphase arrest of non-activated oocytes and Cdc2 itself is required for correct spindle morphology in female meiosis. Cdc2, its subunit, Cks30A, and its regulators, Weel and Twine, are all required for ancentrosomal spindle formation. Cdc2 is a central figure in a kinase pathway required for multiple facets of acentrosomal spindle formation. To gain new insights in the formation of female meiotic spindles I took part in a screen for metaphase I arrested spindle mutants in female meiosis on the X chromosome of Drosophila. I found mutants defective in chromosome alignment, spindle morphology, spindle unification and spindle formation around individual chromosomes. I characterised several of the mutants found in this screen as well as established complementation groups for all of the mutants discovered to aid in future studies.