In Aspergillus nidulans, nimODbf4 is the regulatory subunit of Dbf4 dependent kinase (DDK), which acts to trigger DNA synthesis at origins of replication. The nimO18 mutation confers temperature sensitive cell cycle arrest at G1/S, and at permissive temperature exhibits profound sensitivity to agents that cause double strand breaks (DSBs), such as Phleomycin (PHL). We identified a nimO18 suppressor, called snoA (suppressor-of-nimO), by mutations that rescued nimO18 ts-lethality. Intriguingly, loss of snoA function also substantially protects nimO18 from PHL, restoring near-wild type PHL-resistance. By examining the response of nimO18 to acute versus chronic PHL exposure, I was able to determine that the PHL sensitivity of nimO18 results from a defect in DNA repair, rather than by disabling a DNA damage checkpoint. I am examining how replication and repair processes may be perturbed by examining the recovery of mutants after induction of the S phase DNA replication checkpoint via hydroxyurea (HU) block-release experiments. Surprisingly, although nimO18 grows ~20% more slowly than WT, nimO18 mutants recover more quickly from HU-induced S phase arrest, and loss of snoA in turn slows this recovery. I am using a similar approach to determine how nimO18 and snoA mutants recover from DNA damage incurred during S phase.