Given the role of TORC1 signaling in telomere maintenance and the DDR, and the potential connection of the upstream TORC1 regulator Sea3 with telomere and DNA repair proteins, we sought to determine whether Sea3 played a regulatory role in these processes. We found that deletion of SEA3 did not impact telomere length in telomerase-positive strains but did alter the progression of senescence in the absence of telomerase and delayed the emergence of telomerase-independent survivors that maintain their telomeres via break-induced replication (BIR). Similarly, sea3Δ mutants had a delay in colony formation after DSB induction in a strain that assays for BIR and upon exposure to the DNA-damaging agent bleomycin. We found Sea3 to function, as predicted, upstream of TORC1 through Iml1 after DSB induction. The studies unveil a novel type of recovery defect, which is not in the termination of the DDR, but rather in intracellular tryptophan. They implicate tight regulation of TORC1 signaling via Sea3 in the ability of the cell to achieve sufficient intracellular tryptophan to allow timely recovery after DNA damage.