Therefore, we examined whether tryptophan availability was contributing to the sea3∆ mutant phenotype. Even in rich media, the level of tryptophan is low (measured 26 µg/mL in Jarolim et al. 2013), so we reasoned that if tryptophan availability were the source of the delay in colony formation in the sea3Δ mutant, addition of an excessive amount of tryptophan to the media might rescue the delay. Although we found that both wild-type and sea3∆ mutant strains grew slightly more robustly on YPGal supplemented with an additional 100 μM tryptophan compared with YPGal, the sea3Δ mutant still displayed a growth delay relative to the wild-type (Figure 5B). Combined with the rescue of TRP1 expression, this suggested that after DNA damage, sea3Δ mutants are either unable to import tryptophan into the cell sufficiently or that tryptophan consumption was altered.