Tyrrell R M
Mutat Res. 1978 Oct;52(1):25-35. doi: 10.1016/0027-5107(78)90092-1.
The mutational interaction between radiation at 365 and 254 nm was studied in various strains of E. coli by a mutant assay based on reversion to amino-acid independence in full nutrient conditions. In the two repair-proficient strains (K12 AB 1157 and B/r), pre-treatment with radiation at 365 nm strongly suppressed the induction of mutations by far-UV, a phenomenon accompanied by a strong lethal interaction. The frequency of mutations induced by far-UV progressively declined with increasing dose of near-UV. Far-UV-induced mutagenesis to T5 resistance was almost unaltered by pre-treatment with near-UV. In AB 1886 uvrA there was no lethal interaction between the two wavelengths but the mutagenic interaction was synergistic. This synergism was maximal at a 365-nm dose of 8 X 10(5) J m-2. It is proposed that in the wild-type strain, cells containing potentially mutagenic lesions are selectively eliminated from the population because of abortive excision of an error-prone repair-inducing signal. In excisionless strains, 365-nm radiation may be less damaging to the error-prone than to the error-free post-replication repair system. Alternatively, mutation may be enhanced because of the occurrence of error-prone repair of 365-nm lesions by a system that is not induced in the absence of 254-nm radiation.
通过一种基于在完全营养条件下回复到氨基酸非依赖状态的突变检测方法，研究了365纳米和254纳米辐射在大肠杆菌不同菌株中的突变相互作用。在两个修复能力正常的菌株（K12 AB 1157和B/r）中，用365纳米辐射预处理可强烈抑制远紫外线诱导的突变，这一现象伴随着强烈的致死相互作用。远紫外线诱导的突变频率随着近紫外线剂量的增加而逐渐下降。近紫外线预处理对远紫外线诱导的对T5抗性的诱变作用几乎没有影响。在AB 1886 uvrA中，两个波长之间没有致死相互作用，但诱变相互作用是协同的。这种协同作用在365纳米剂量为8×10⁵ J m⁻²时最大。有人提出，在野生型菌株中，含有潜在诱变损伤的细胞由于易错修复诱导信号的流产性切除而从群体中被选择性清除。在无切除修复的菌株中，365纳米辐射对易错修复系统的损害可能比对无错复制后修复系统的损害小。或者，由于在没有254纳米辐射时不被诱导的系统对365纳米损伤进行易错修复，可能会增强突变。
