在实验室中，研究人员经常将细胞暴露于高剂量的紫外线，以测量它们对DNA损伤的反应。但在有机体暴露于连续的或间歇的低剂量紫外线的真实世界中会发生什么情况呢？
关于环境相关的紫外线水平对酵母细胞的影响的一项研究工作表明，细胞中存在一个DNA系统，该系统很敏感，足以在暴露于低剂量紫外线之后产生反应。
这个系统即RAD6-RAD8-RAD5复制后修复通道。当复制叉被中断时，通过阻止过量单链DNA的产生，它允许细胞在其DNA受损时对其进行复制，从而避免会抑制增殖的一个细胞反应的激发。(生物谷Bioon.com)
生物谷推荐原始出处：
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.
