在實(shí)驗(yàn)室中,，研究人員經(jīng)常將細(xì)胞暴露于高劑量的紫外線,，以測(cè)量它們對(duì)DNA損傷的反應(yīng)。但在有機(jī)體暴露于連續(xù)的或間歇的低劑量紫外線的真實(shí)世界中會(huì)發(fā)生什么情況呢,？
關(guān)于環(huán)境相關(guān)的紫外線水平對(duì)酵母細(xì)胞的影響的一項(xiàng)研究工作表明,，細(xì)胞中存在一個(gè)DNA系統(tǒng)，該系統(tǒng)很敏感,，足以在暴露于低劑量紫外線之后產(chǎn)生反應(yīng),。
這個(gè)系統(tǒng)即RAD6-RAD8-RAD5復(fù)制后修復(fù)通道。當(dāng)復(fù)制叉被中斷時(shí),，通過(guò)阻止過(guò)量單鏈DNA的產(chǎn)生,，它允許細(xì)胞在其DNA受損時(shí)對(duì)其進(jìn)行復(fù)制，從而避免會(huì)抑制增殖的一個(gè)細(xì)胞反應(yīng)的激發(fā),。(生物谷Bioon.com)
生物谷推薦原始出處：
Nature 457, 612-615 (29 January 2009) | doi:10.1038/nature07580
RAD6–RAD18–RAD5-pathway-dependent tolerance to chronic low-dose ultraviolet light
Takashi Hishida1, Yoshino Kubota1, Antony M. Carr2 & Hiroshi Iwasaki3
1 Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan
2 MRC Genome Damage and Stability Centre, University of Sussex, Brighton BN1 9RQ, UK
3 International Graduate School of Arts and Sciences, Yokohama City University, 1-7-29, Suehiro, Tsurumi, Yokohama, Kanagawa 230-0045, Japan
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 pathway1 and for checkpoint-induced cell cycle arrest in promoting cell survival2. 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) pathway3, 4 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 foci5 in the CLUV-exposed rad18 cells and demonstrated that Rad52-mediated homologous recombination is required for the viability of the rad18 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.
