Tanaka Masashi, Narumi Issay, Funayama Tomoo, Kikuchi Masahiro, Watanabe Hiroshi, Matsunaga Tsukasa, Nikaido Osamu, Yamamoto Kazuo
Department of Biomolecular Sciences, Graduate School of Life Sciences, Tohoku University, Sendai 980-8577, Japan.
J Bacteriol. 2005 Jun;187(11):3693-7. doi: 10.1128/JB.187.11.3693-3697.2005.
The genome of a radiation-resistant bacterium, Deinococcus radiodurans, contains one uvsE gene and two uvrA genes, uvrA1 and uvrA2. Using a series of mutants lacking these genes, we determined the biological significance of these components to UV resistance. The UV damage endonuclease (UvsE)-dependent excision repair (UVER) pathway and UvrA1-dependent pathway show some redundancy in their function to counteract the lethal effects of UV. Loss of these pathways does not cause increased sensitivity to UV mutagenesis, suggesting either that these pathways play no function in inducing mutations or that there are mechanisms to prevent mutation other than these excision repair pathways. UVER efficiently removes both cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs) from genomic DNA. In contrast, the UvrA1 pathway does not significantly contribute to the repair of CPDs but eliminates 6-4PPs. Inactivation of uvrA2 does not result in a deleterious effect on survival, mutagenesis, or the repair kinetics of CPDs and 6-4PPs, indicating a minor role in resistance to UV. Loss of uvsE, uvrA1, and uvrA2 reduces but does not completely abolish the ability to eliminate CPDs and 6-4PPs from genomic DNA. The result indicates the existence of a system that removes UV damage yet to be identified.
耐辐射细菌耐辐射球菌的基因组包含一个uvsE基因和两个uvrA基因，即uvrA1和uvrA2。我们利用一系列缺失这些基因的突变体，确定了这些组分对紫外线抗性的生物学意义。紫外线损伤内切酶（UvsE）依赖性切除修复（UVER）途径和UvrA1依赖性途径在对抗紫外线致死效应的功能上表现出一定的冗余性。这些途径的缺失不会导致对紫外线诱变的敏感性增加，这表明要么这些途径在诱导突变中不起作用，要么存在除这些切除修复途径之外的防止突变的机制。UVER能有效地从基因组DNA中去除环丁烷嘧啶二聚体（CPD）和嘧啶（6-4）嘧啶酮光产物（6-4PP）。相比之下，UvrA1途径对CPD的修复没有显著贡献，但能消除6-4PP。uvrA2的失活不会对存活、诱变或CPD和6-4PP的修复动力学产生有害影响，表明其在抗紫外线方面作用较小。uvsE、uvrA1和uvrA2的缺失会降低但不会完全消除从基因组DNA中去除CPD和6-4PP的能力。结果表明存在一个尚未被鉴定的去除紫外线损伤的系统。
