Source:http://linkedlifedata.com/resource/pubmed/id/18677117
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
15
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pubmed:dateCreated |
2008-8-8
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pubmed:abstractText |
Specific ataxia telangiectasia and Rad3-related (ATR) mutations confer higher frequencies of homologous recombination. The genetic requirements for hyper-recombination in ATR mutants are unknown. MEC1, the essential yeast ATR/ATM homolog, controls S and G(2) checkpoints and the DNA damage-inducibility of genes after radiation exposure. Since the mec1-Delta (null) mutant is defective in both S and G(2) checkpoints, we measured spontaneous and DNA damage-associated sister chromatid exchange (SCE), homolog (heteroallelic) recombination, and homology-directed translocations in the mec1-21 hypomorphic mutant, which is defective in the S phase checkpoint but retains some G(2) checkpoint function. We observed a sixfold, tenfold and 30-fold higher rate of spontaneous SCE, heteroallelic recombination, and translocations, respectively, in mec1-21 mutants compared to wild type. The mec1-21 hyper-recombination was partially reduced in rad9, pds1 and chk1 mutants, and abolished in rad52 mutants, suggesting the hyper-recombination results from RAD52-dependent recombination pathway(s) that require G(2) checkpoint functions. The HU and UV sensitivities of mec1-21 rad9 and mec1-21 rad52 were synergistically increased, compared to the single mutants, indicating that mec1-21, rad52 and rad9 mutants are defective in independent pathways for HU and UV resistance. G(2)-arrested mec1-21 rad9 cells exhibit more UV resistance than non-synchronized cells, indicating that one function of RAD9 in conferring UV resistance in mec1-21 is by triggering G(2) arrest. We suggest that checkpoint genes that function in the RAD9-mediated pathway are required for either homologous recombination or DNA damage resistance in the S phase checkpoint mutant mec1-21.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cell Cycle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Checkpoint kinase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/MEC1 protein, S cerevisiae,
http://linkedlifedata.com/resource/pubmed/chemical/Mutant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/PDS1 protein, S cerevisiae,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/RAD52 protein, S cerevisiae,
http://linkedlifedata.com/resource/pubmed/chemical/Rad52 DNA Repair and Recombination...,
http://linkedlifedata.com/resource/pubmed/chemical/Saccharomyces cerevisiae Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/rad9 protein
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1551-4005
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
7
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2418-26
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pubmed:dateRevised |
2011-11-2
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pubmed:meshHeading |
pubmed-meshheading:18677117-Cell Cycle Proteins,
pubmed-meshheading:18677117-G2 Phase,
pubmed-meshheading:18677117-Genes, cdc,
pubmed-meshheading:18677117-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:18677117-Models, Biological,
pubmed-meshheading:18677117-Mutant Proteins,
pubmed-meshheading:18677117-Nuclear Proteins,
pubmed-meshheading:18677117-Organisms, Genetically Modified,
pubmed-meshheading:18677117-Phenotype,
pubmed-meshheading:18677117-Protein Kinases,
pubmed-meshheading:18677117-Protein-Serine-Threonine Kinases,
pubmed-meshheading:18677117-Rad52 DNA Repair and Recombination Protein,
pubmed-meshheading:18677117-Recombination, Genetic,
pubmed-meshheading:18677117-Saccharomyces cerevisiae,
pubmed-meshheading:18677117-Saccharomyces cerevisiae Proteins,
pubmed-meshheading:18677117-Sequence Homology
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pubmed:year |
2008
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pubmed:articleTitle |
The Saccharomyces cerevisiae checkpoint genes RAD9, CHK1 and PDS1 are required for elevated homologous recombination in a mec1 (ATR) hypomorphic mutant.
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pubmed:affiliation |
Ordway Research Institute, Albany, New York 12208, USA. mfasullo@ordwayresearch.org
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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