Abstract
Telomerase-deficient Saccharomyces cerevisiae cells show a progressive decrease in telomere length. When grown for several days in log phase, the tlc1Delta cells initially display wild-type growth kinetics with subsequent loss of growth potential after which survivors are generated via RAD52-dependent homologous recombination. We found that chromosome loss in these telomerase-deficient cells only increased after a significant decline in growth potential of the culture. At earlier stages of growth, as the telomerase-deficient cells began to show loss of growth potential, the cells arrested in G2/M and showed RNR3 induction and Rad53p phosphorylation. These responses were dependent on RAD24 and MEC1, suggesting that short telomeres are recognized as DNA damage and signal G2/M arrest.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Cell Cycle / physiology*
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Cell Cycle Proteins / genetics
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Cell Cycle Proteins / metabolism
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Cell Division / physiology
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DNA Damage
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism
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Intracellular Signaling Peptides and Proteins
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Protein Serine-Threonine Kinases
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Rad52 DNA Repair and Recombination Protein
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Saccharomyces cerevisiae / genetics*
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Saccharomyces cerevisiae / metabolism
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Saccharomyces cerevisiae Proteins / genetics
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Saccharomyces cerevisiae Proteins / metabolism
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Telomerase / genetics
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Telomerase / metabolism*
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Telomere / metabolism*
Substances
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Cell Cycle Proteins
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DNA-Binding Proteins
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Intracellular Signaling Peptides and Proteins
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RAD24 protein, S cerevisiae
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RAD52 protein, S cerevisiae
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Rad52 DNA Repair and Recombination Protein
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Saccharomyces cerevisiae Proteins
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MEC1 protein, S cerevisiae
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Protein Serine-Threonine Kinases
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Telomerase