Ishii Y, Kondo S
Mutat Res. 1975 Jan;27(1):27-44. doi: 10.1016/0027-5107(75)90271-7.
Dose-response curves were compared for deletions [ColBR (resistant to colicin B) mutations being more than 80% deletions] and base changes (reversion of argFam to prototrophy argplus) induced in the same set of E. coli strains (wild-type for DNA repair, uvrA-, polA- and recA-) by N-methyl-N'-nitro-N-nitrosoguanidine (NTG), ethyl methanesulfonate (EMS), hydroxylamine (HA), 4-nitroquinoline I-oxide (4NQO), mitomycin C (MTC, UV and X-rays. All these agents induced deletions as well as base changes in the wild-type strain. Thus chemical mutagenesis differed in E. coli and bacteriophages in vitro, for HA, NTG, EMS and perhaps UV produced only point mutations in phage Tr. The patterns of deletion and base-change mutability in E. coli were surprisingly similar. (I) The recombination less recA- strain was mutable by only three (NTG, EMS, HA) of the seven mutagens for either deletions or base changes. (2) The uvrA- strain, unable to excise pyrimidine dimers, was very highly mutable by 4NQO and UV but immutable by MTC for both deletions and base changes. (3) The polA- strain, defective in DNA polymerase I due to a non-suppressible mutation, was very highly mutable by HA and highly mutable by MTC and 4NQO for both deletions and base changes but was highly mutable only for deletions by UV and X-rays, remaining normally mutable by the other agents for both deletions and base changes despite its high sensitivity to their inactivating action. We conclude that errors in the recA-dependent repair of induced DNA damage (after 4NQO, MTC, UV and X-rays) or errors in replication enhanced by damage to the replication system or to the template strands (after NTG, EMS, and HA) give rise to deletions as well as to base changes. From a comparative analysis of 14 dose-response curves for deletions and base changes, we conclude that the order of mutagenic efficiency relative to killing is (EMS, NTG) greater than (UV, 4NQO) greater than HA greater than (X-rays, MTC), and that X-rays, 4NQO, HA and MTC induce more ColBR deletions than Argplus base changes, whereas UV and EMS induce ColBR deletions and Argplus base changes at nearly equal rates and the specificity of NTG is intermediate between these two types.
比较了在同一组大肠杆菌菌株（DNA修复野生型、uvrA -、polA -和recA -）中，由N -甲基 - N' -硝基 - N -亚硝基胍（NTG）、甲磺酸乙酯（EMS）、羟胺（HA）、4 -硝基喹啉 - N -氧化物（4NQO）、丝裂霉素C（MTC）、紫外线（UV）和X射线诱导产生的缺失（ColBR（对大肠杆菌素B有抗性）突变中超过80%为缺失）和碱基变化（argFam回复为原养型argplus）的剂量 - 反应曲线。所有这些诱变剂在野生型菌株中都能诱导缺失和碱基变化。因此，大肠杆菌中的化学诱变与体外噬菌体中的不同，因为HA、NTG、EMS以及可能的UV在噬菌体Tr中仅产生点突变。大肠杆菌中缺失和碱基变化的诱变模式惊人地相似。（1）重组缺陷型recA -菌株对于七种诱变剂中的三种（NTG、EMS、HA），无论是缺失还是碱基变化都具有诱变作用。（2）uvrA -菌株无法切除嘧啶二聚体，对4NQO和UV的诱变作用非常敏感，但对MTC的缺失和碱基变化都不敏感。（3）polA -菌株由于不可抑制的突变导致DNA聚合酶I缺陷，对HA的诱变作用非常敏感，对MTC和4NQO的缺失和碱基变化都高度敏感，但对UV和X射线仅在缺失方面高度敏感，尽管对它们的灭活作用高度敏感，但对其他诱变剂的缺失和碱基变化仍正常敏感。我们得出结论，诱导的DNA损伤（4NQO、MTC、UV和X射线处理后）的recA依赖性修复中的错误，或复制系统或模板链损伤增强的复制中的错误（NTG、EMS和HA处理后）会导致缺失和碱基变化。通过对14条缺失和碱基变化的剂量 - 反应曲线的比较分析，我们得出结论，相对于杀伤作用而言，诱变效率的顺序为（EMS、NTG）大于（UV、4NQO）大于HA大于（X射线、MTC），并且X射线、4NQO、HA和MTC诱导的ColBR缺失比Argplus碱基变化更多，但UV和EMS诱导ColBR缺失和Argplus碱基变化的速率几乎相等且NTG的特异性介于这两种类型之间。
