Cited by 370DNA Repair MechanismsFungal and yeast genetics researchBacterial Genetics and Biotechnology

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

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Morrow, Dwight M, Tagle, Danilo A, Shiloh, Yosef, Collins, Francis S, Hieter, Philip·1995·Cell

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.

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Crossref · 10.1016/0092-8674(95)90480-8

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  • In budding yeast, Mec1 is the main checkpoint activator after all DNA lesions, while Tel1 is mainly devoted to telomere maintenance; Tel1's redundant checkpoint role appears only without Mec1.

    “This separation of tasks is not found in budding yeast, where Mec1 (the ATR homologue) is the main player of checkpoint activation after all kind of DNA lesions, while Tel1 (the ATM homologue) is especially devoted to telomere maintenance. The redundant role of Tel1 in the DNA damage checkpoint is uncovered only in the absence of Mec1 [15,43].”

    From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [43]

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Authors
Morrow, D. M., Tagle, D. A., Shiloh, Y., Collins, F. S., & Hieter, P.
Affiliations
  • Johns Hopkins University (US)
  • National Institutes of Health (US)
  • Tel Aviv University (IL)
Venue
Cell
Publisher
Elsevier BV
Published
1995-09
Volume
82
Issue
5
Pages
831-840
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2028263332
Cited by
370
References
58
Citations by year
2026: 1 · 2025: 2 · 2024: 3 · 2023: 2 · 2022: 3 · 2021: 1 · 2020: 7 · 2019: 5 · 2018: 4 · 2017: 5 · 2016: 9 · 2015: 8 · 2014: 6 · 2013: 8 · 2012: 7
FWCI
14.99
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
  • U.S. Department of Energy
  • National Institute for Health and Care Research
  • Ministerio de Economía y Competitividad
  • National Institutes of Health
  • National Cancer Institute (CA-16519, P01CA016519)
  • National Institute of General Medical Sciences (GM162283)
  • National Institute of Neurological Disorders and Stroke (R01NS031763, NS 31763)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
Keywords
Tel1, Mec1, ataxia telangiectasia, ATM gene, DNA damage checkpoint, radiomimetic drugs, dosage compensation, Saccharomyces cerevisiae
MeSH terms
Ataxia Telangiectasia, Base Sequence, Bleomycin, Cloning, Molecular, DNA Damage, Fungal Proteins, Gamma Rays, Genes, Fungal, Humans, Hydroxyurea, Molecular Sequence Data, Mutation, Phenotype, Saccharomyces cerevisiae, Streptonigrin, Ultraviolet Rays, Protein Serine-Threonine Kinases, Sequence Homology, Amino Acid, Saccharomyces cerevisiae Proteins, Intracellular Signaling Peptides and Proteins

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