TY - JOUR
T1 - TEL1, an S. cerevisiae homolog of the human gene mutated in ataxia telangiectasia, is functionally related to the yeast checkpoint gene MEC1
AU - Morrow, Dwight M.
AU - Tagle, Danilo A.
AU - Shiloh, Yosef
AU - Collins, Francis S.
AU - Hieter, Philip
N1 - Funding Information:
Correspondence should be addressed to F. S. C. D. M. M. thanks his wife, M. Holland, for her love and support during this work, her technical assistance, and her assistance in preparing this manuscript. We would like to thank T. Petes and T. Pandita for making preprints available, T. Petes and J. Lamb for helpful discussions, and T. Weinert for providing the mec 1-1 strain. D. M. M. is supported in part by a National Research Service Award (grant GM162283). Y. S., D. A. T., and F. S. C. are supported in part by the United States-Israel Binational Science Foundation, the United States Department of Energy (grants FG0387 and ERL0548), and the National Institute of Neurological Disorders and Stroke (grant NS31763 to Y. S.). P. H. is supported in part by the National Institutes of Health (grants CA16519 and HG00971).
PY - 1995/9/8
Y1 - 1995/9/8
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0029150855&partnerID=8YFLogxK
U2 - 10.1016/0092-8674(95)90480-8
DO - 10.1016/0092-8674(95)90480-8
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
AN - SCOPUS:0029150855
SN - 0092-8674
VL - 82
SP - 831
EP - 840
JO - Cell
JF - Cell
IS - 5
ER -