Both the SEA complex and TORC1 signaling have been linked to amino acid biosynthesis and internal trafficking of amino acid permeases. In the case of the SEA complex, the link has been inferred from genome-wide pairwise fitness screen data (Beck et al. 1999; Dokudovskaya et al. 2011; Schmidt et al. 1998). Therefore, it was possible that the delay in colony formation after DNA damage was attributable to a change in amino acid requirements. The parental BIR assay strain is auxotrophic for the amino acids tryptophan and leucine as well as the nucleobase uracil due to trp1, leu2, and ura3 mutations, respectively. Therefore, we asked whether addition of wild-type copies of these genes impacted the growth of wild-type and sea3Δ mutant strains. Introduction of a LEU2 CEN plasmid into the parental wild-type BIR assay strain did not result in a growth delay upon plating on galactose (Figure S6A), whereas deletion of SEA3 with a kanMX cassette did (Figure S6B), indicating that the growth delay of the sea3Δ::LEU2 mutant BIR strain on galactose was not due to LEU2 expression. Surprisingly, however, introduction of a TRP1 CEN plasmid rescued the delay of the sea3∆ mutant (Figure 5A). The rescue was specific to TRP1, as introduction of a URA3 CEN plasmid did not similarly rescue the delay (Figure S3A). Likewise, TRP1 rescued the growth delay observed when the sea3∆::HPH mutant in the YPH274 (trp1-) background was plated on bleomycin, although to a partial extent (Figure S7). These results suggested that the delay in colony formation observed in sea3∆ mutants was due to perturbations in internal levels of tryptophan.