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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
15
pubmed:dateCreated
2008-8-8
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
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
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2418-26
pubmed:dateRevised
2011-11-2
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
pubmed:year
2008
pubmed:articleTitle
The Saccharomyces cerevisiae checkpoint genes RAD9, CHK1 and PDS1 are required for elevated homologous recombination in a mec1 (ATR) hypomorphic mutant.
pubmed:affiliation
Ordway Research Institute, Albany, New York 12208, USA. mfasullo@ordwayresearch.org
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural