Linked Life Data

19079240

Source:http://linkedlifedata.com/resource/pubmed/id/19079240

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7229
pubmed:dateCreated
2009-1-29
pubmed:abstractText
In nature, organisms are exposed to chronic low-dose ultraviolet light (CLUV) as opposed to the acute high doses common to laboratory experiments. Analysis of the cellular response to acute high-dose exposure has delineated the importance of direct DNA repair by the nucleotide excision repair pathway and for checkpoint-induced cell cycle arrest in promoting cell survival. Here we examine the response of yeast cells to CLUV and identify a key role for the RAD6-RAD18-RAD5 error-free postreplication repair (RAD6 error-free PRR) pathway in promoting cell growth and survival. We show that loss of the RAD6 error-free PRR pathway results in DNA-damage-checkpoint-induced G2 arrest in CLUV-exposed cells, whereas wild-type and nucleotide-excision-repair-deficient cells are largely unaffected. Cell cycle arrest in the absence of the RAD6 error-free PRR pathway was not caused by a repair defect or by the accumulation of ultraviolet-induced photoproducts. Notably, we observed increased replication protein A (RPA)- and Rad52-yellow fluorescent protein foci in the CLUV-exposed rad18Delta cells and demonstrated that Rad52-mediated homologous recombination is required for the viability of the rad18Delta cells after release from CLUV-induced G2 arrest. These and other data presented suggest that, in response to environmental levels of ultraviolet exposure, the RAD6 error-free PRR pathway promotes replication of damaged templates without the generation of extensive single-stranded DNA regions. Thus, the error-free PRR pathway is specifically important during chronic low-dose ultraviolet exposure to prevent counter-productive DNA checkpoint activation and allow cells to proliferate normally.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphatases, http://linkedlifedata.com/resource/pubmed/chemical/DNA, Fungal, http://linkedlifedata.com/resource/pubmed/chemical/DNA Helicases, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/RAD18 protein, S cerevisiae, http://linkedlifedata.com/resource/pubmed/chemical/RAD5 protein, S cerevisiae, http://linkedlifedata.com/resource/pubmed/chemical/RAD52 protein, S cerevisiae, http://linkedlifedata.com/resource/pubmed/chemical/RAD6 protein, S cerevisiae, http://linkedlifedata.com/resource/pubmed/chemical/Rad52 DNA Repair and Recombination..., http://linkedlifedata.com/resource/pubmed/chemical/Replication Protein A, http://linkedlifedata.com/resource/pubmed/chemical/Saccharomyces cerevisiae Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Ubiquitin-Conjugating Enzymes
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1476-4687
pubmed:author
pubmed:issnType
Electronic
pubmed:day
29
pubmed:volume
457
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
612-5
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
RAD6-RAD18-RAD5-pathway-dependent tolerance to chronic low-dose ultraviolet light.
pubmed:affiliation
Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan. hishida@biken.osaka-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't