Norin A J, Goldschmidt E P
Mutat Res. 1979 Jan;59(1):15-26. doi: 10.1016/0027-5107(79)90191-x.
The ability of mutagenic agents, nonmutagenic substances and defects in DNA repair to alter the genotype of F' partial diploid (F30) Escherichia coli was determined. The frequency of auxotrophic mutants and histidine requiring (His-) haploid colonies was increased by mutagen treatment but Hfr colonies were not detected in F30 E. coli even with specific selection techniques. Genotype changes due to nonreciprocal recombination were determined by measuring the frequency of His- homogenotes, eg. F' hisC780, hisI+/hisC780, hisI+, arising from a His+ heterogenote, F' hisC780 hisI+/hisC+, his1903. At least 75% of the recombinants were homozygous for histidine alleles which were present on the F' plasmid (exogenote) of the parental hetergenote rather than for histidine alleles on the chromosome. Mutagens, chemotherapeutic agents which histidine alleles on the chromosome. Mutagens, chemotherapeutic agents which block DNA synthesis and a defective DNA polymerase I gene, polA1, were found to increase the frequency of nonreciprocal recombination. A defect in the ability to excise thymine dimers, uvrC34, did not increase spontaneous nonreciprocal recombination. However, UV irradiation but not methyl methanesulfonate (MMS) induced greater recombination in this excision-repair defective mutant than in DNA-repair-proficient strains. Mutagenic agents, with the exception of ethyl methanesulfonate (EMS), induced greater increases in recombination than the chemotherapeutic agents or the polA1 mutation. EMS, which causes relatively little degradation of DNA, was more mutagenic but less recombinogenic than MMS, a homologous compound ths that inhibition of DNA occurring single-stranded regions in replicative intermediates of the DNA. Mutagens which cause the rapid breakdown of DNA may, in addition, introduce lesions into the genome that increase the number of single-stranded regions thus inducing even higher frequencies of recombination.
测定了诱变剂、非诱变物质以及DNA修复缺陷对F'部分二倍体（F30）大肠杆菌基因型的改变能力。诱变处理增加了营养缺陷型突变体和组氨酸需求型（His-）单倍体菌落的频率，但即使采用特定的选择技术，在F30大肠杆菌中也未检测到高频重组（Hfr）菌落。通过测量His-纯合子的频率来确定由于非相互重组导致的基因型变化，例如，F' hisC780、hisI+/hisC780、hisI+源自His+异源合子F' hisC780 hisI+/hisC+、his1903。至少75%的重组体对于亲本异源合子F'质粒（外基因子）上存在的组氨酸等位基因是纯合的，而非染色体上的组氨酸等位基因。发现诱变剂、阻断DNA合成的化疗药物以及有缺陷的DNA聚合酶I基因polA1会增加非相互重组的频率。切除胸腺嘧啶二聚体能力的缺陷uvrC34并没有增加自发非相互重组的频率。然而，紫外线照射而非甲磺酸甲酯（MMS）在这种切除修复缺陷型突变体中诱导的重组比在DNA修复 proficient菌株中更多。除甲磺酸乙酯（EMS）外，诱变剂诱导的重组增加幅度比化疗药物或polA1突变更大。EMS导致的DNA降解相对较少，其诱变作用更强，但重组作用比同源化合物MMS弱，MMS抑制DNA复制中间体单链区域的DNA。此外，导致DNA快速分解的诱变剂可能会在基因组中引入损伤，增加单链区域的数量，从而诱导更高频率的重组。
