The tryptophan auxotrophy-dependent delay in colony formation in the sea3∆ BIR assay strain on rich, but not synthetic, media (Figure S8) is reminiscent of the growth phenotype of yeast with mutations in ELM1, which encodes a serine/threonine kinase involved in cell growth and division (Garrett 1997). In previous studies, elm1 mutant strains were found to have a different set of phenotypes depending on whether they were auxotrophic or prototrophic for tryptophan. In addition, the elm1 mutant phenotype was observed on rich media but not on synthetic defined media containing tryptophan. Examination of the activity of several amino acid permeases revealed Gap1 activity was inappropriately decreased in cells deficient in both Elm1 and internal tryptophan. Thus, rather than Tat2, misregulation of Gap1, a known target of TORC1 signaling, may be responsible for the delay in colony formation upon DNA damage in the sea3∆ mutant. Indeed, a delay in colony formation upon DNA damage was not observed in the tat2∆ strain (Figure S10), indicating an alternate pathway for tryptophan import upon DNA damage.