The deacetylase inhibitor, TSA, alleviates the persistent checkpoint delay in yng2 mutants. Wild-type (YNG2) and yng2 mutant cells were pretreated with 30 μg of TSA/ml overnight (+MMS +TSA) or left untreated (+MMS) prior to addition of αf to induce G1 arrest. MMS was added to a final concentration of 0.03% while cells were in G1 for 45 min, αf was washed away, and cells were allowed to enter the cell cycle in the presence of 0.03% MMS with or without TSA. While YNG2 cells progress through S phase in MMS alone or MMS and TSA, yng2 mutants persist in S phase when treated with MMS but progress through S phase when TSA is present. No MMS, cells not treated with MMS.