TEL1, an S. cerevisiae homolog of the human gene mutated in ataxia telangiectasia, is functionally related to the yeast checkpoint gene MEC1

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,...

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Bibliographic Details
Published in:Cell 1995-09, Vol.82 (5), p.831-840
Main Authors: Morrow, Dwight M, Tagle, Danilo A, Shiloh, Yosef, Collins, Francis S, Hieter, Philip
Format: Article
Language:English
Subjects:
Ataxia Telangiectasia - genetics
Base Sequence
Bleomycin - pharmacology
Cloning, Molecular
DNA Damage - genetics
DNA Damage - radiation effects
Fungal Proteins - genetics
Gamma Rays
Genes, Fungal - physiology
Humans
Hydroxyurea
Intracellular Signaling Peptides and Proteins
Molecular Sequence Data
Mutation - genetics
Mutation - radiation effects
Phenotype
Protein-Serine-Threonine Kinases
Saccharomyces cerevisiae
Saccharomyces cerevisiae - genetics
Saccharomyces cerevisiae Proteins
Sequence Homology, Amino Acid
Streptonigrin - pharmacology
Ultraviolet Rays
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Summary: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.
ISSN:0092-8674
1097-4172
DOI:10.1016/0092-8674(95)90480-8