Patients with the genetic disorder ataxia telangiectasia (AT) have mutations in the AT mutated (ATM) gene, which is homologous to TELI and the checkpoint gene MEC1. A tel1 deletion mutant, unlike a mec1 deletion, is viable and does not exhibit increased sensitivity to DNA-damaging agents. However, increased dosage of TEL1 rescues sensitivity of a mec1 mutant, mec1-1, to DNA-damaging agents and rescues viability of a mec1 disruption. mecl-1 tel1Δl double mutants are synergistically sensitive to DNA-damaging agents, including radiomimetic drugs. These data indicate that TEL l and MEC1 are functionally related and that functions of the ATM gene are apparently divided between at least two S. cerevisiae homologs.