Finally, to determine whether the dephosphorylated form of Cas5 was required for controlled DNA replication, we quantified the number of nuclei per cell in the phosphomutants. The CAS5 mutant carrying the phosphomimetic S769E substitution phenocopied the cell cycle defects observed in the CAS5 homozygous deletion mutant, whereas the mutant carrying phosphodeficient S769A substitution was indistinguishable from the wildtype (Fig. 9f). Thus, our results support a novel role for the dephosphorylated form of Cas5 in regulating nuclear division that is largely independent of the SBF complex.