Abstract
Patients with the genetic disorder ataxia telangiectasia (AT) have mutations in the AT mutated (ATM) gene, which is homologous to TEL1 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. mec1-1 tel1 delta 1 double mutants are synergistically sensitive to DNA-damaging agents, including radiomimetic drugs. These data indicate that TEL1 and MEC1 are functionally related and that functions of the ATM gene are apparently divided between at least two S. cerevisiae homologs.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Ataxia Telangiectasia / genetics*
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Base Sequence
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Bleomycin / pharmacology
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Cloning, Molecular
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DNA Damage / genetics
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DNA Damage / radiation effects
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Fungal Proteins / genetics*
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Gamma Rays
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Genes, Fungal / physiology*
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Humans
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Hydroxyurea
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Intracellular Signaling Peptides and Proteins
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Molecular Sequence Data
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Mutation / genetics
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Mutation / radiation effects
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Phenotype
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Protein Serine-Threonine Kinases
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Saccharomyces cerevisiae / genetics*
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Saccharomyces cerevisiae Proteins
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Sequence Homology, Amino Acid
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Streptonigrin / pharmacology
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Ultraviolet Rays
Substances
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Fungal Proteins
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Intracellular Signaling Peptides and Proteins
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Saccharomyces cerevisiae Proteins
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Bleomycin
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Streptonigrin
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Protein Serine-Threonine Kinases
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TEL1 protein, S cerevisiae
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Hydroxyurea