We next looked for possible targets downstream of TORC1 that might be responsible for the delay in colony formation phenotype. Likely candidates were factors mediating autophagy, which is negatively regulated by TORC1 signaling, and previously identified to be a pathway downstream of the yeast SEA complex (Dokudovskaya et al. 2011; Takahara and Maeda 2013). If Sea3 functioned to promote TORC1 repression of autophagy and, thereby, regulate growth post-DNA repair, then a block in autophagy would rescue the delay observed in the sea3∆ mutant. However, we found that deletion of ATG5, which encodes a core autophagy factor (Mizushima et al. 1998), had no impact on the delay in the BIR assay strain (Figure 4C). Thus, the delay in colony formation in the sea3∆ mutant was not due to aberrant up-regulation of autophagy but rather due to misregulation of another downstream TORC1 target.