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タイトル
和文: 
英文:RAD6-RAD18-RAD5-pathway-dependent tolerance to chronic low-dose ultraviolet light 
著者
和文: Hishida, T., Carr, A.M., 岩崎博史.  
英文: Hishida, T., Carr, A.M., Hiroshi Iwasaki.  
言語 English 
掲載誌/書名
和文:Nature 
英文:Nature 
巻, 号, ページ Vol. 457    No. 7229    pp. 612-615
出版年月 2009年1月 
出版者
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会議名称
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開催地
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公式リンク http://www.scopus.com/inward/record.url?eid=2-s2.0-59049087433&partnerID=MN8TOARS
 
DOI https://doi.org/10.1038/nature07580
アブストラクト 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.

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