Document Detail

MEC3, MEC1, and DDC2 are essential components of a telomere checkpoint pathway required for cell cycle arrest during senescence in Saccharomyces cerevisiae.
MedLine Citation:
PMID:  12181334     Owner:  NLM     Status:  MEDLINE    
When telomerase is absent and/or telomeres become critically short, cells undergo a progressive decline in viability termed senescence. The telomere checkpoint model predicts that cells will respond to a damaged or critically short telomere by transiently arresting and activating repair of the telomere. We examined the senescence of telomerase-deficient Saccharomyces cerevisiae at the cellular level to ask if the loss of telomerase activity triggers a checkpoint response. As telomerase-deficient mutants were serially subcultured, cells exhibited a progressive decline in average growth rate and an increase in the number of cells delayed in the G2/M stage of the cell cycle. MEC3, MEC1, and DDC2, genes important for the DNA damage checkpoint response, were required for the cell cycle delay in telomerase-deficient cells. In contrast, TEL1, RAD9, and RAD53, genes also required for the DNA damage checkpoint response, were not required for the G2/M delay in telomerase-deficient cells. We propose that the telomere checkpoint is distinct from the DNA damage checkpoint and requires a specific set of gene products to delay the cell cycle and presumably to activate telomerase and/or other telomere repair activities.
Shinichiro Enomoto; Lynn Glowczewski; Judith Berman
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Molecular biology of the cell     Volume:  13     ISSN:  1059-1524     ISO Abbreviation:  Mol. Biol. Cell     Publication Date:  2002 Aug 
Date Detail:
Created Date:  2002-08-15     Completed Date:  2003-04-09     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9201390     Medline TA:  Mol Biol Cell     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2626-38     Citation Subset:  IM    
Department of Genetics, Cell Biology and Development, University of Minnesota, St. Paul 55108, USA.
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MeSH Terms
Adaptor Proteins, Signal Transducing
Cell Cycle / physiology*
Cell Cycle Proteins / genetics,  metabolism*
DNA Damage
Fungal Proteins / metabolism
Genes, cdc
Intracellular Signaling Peptides and Proteins
Phosphoproteins / genetics,  metabolism*
Protein-Serine-Threonine Kinases / metabolism
Saccharomyces cerevisiae / cytology,  physiology*
Saccharomyces cerevisiae Proteins / genetics,  metabolism*
Telomerase / metabolism
Telomere / metabolism*
Grant Support
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Cell Cycle Proteins; 0/Fungal Proteins; 0/Intracellular Signaling Peptides and Proteins; 0/LCD1 protein, S cerevisiae; 0/MEC3 protein, S cerevisiae; 0/Phosphoproteins; 0/Saccharomyces cerevisiae Proteins; 139691-42-2/rad9 protein; EC 2.7.1.-/RAD53 protein, S cerevisiae; EC protein, S cerevisiae; EC Kinases; EC protein, S cerevisiae; EC

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