Sargentini N J, Smith K C
Mutat Res. 1986 Jul;161(2):113-8. doi: 10.1016/0027-5107(86)90002-3.
In search of a model for the production of 'spontaneous' mutations induced by DNA damage produced during normal metabolism, 19 amino acids were tested for mutagenicity in Escherichia coli K-12 uvrB. Cystine, and, to a lesser extent, arginine and threonine were found to be antimutagenic; only phenylalanine was found to be mutagenic. At 2 mM, phenylalanine induced mutants at 1.5-2-fold above background [lacZ53(amber)----Lac+, rifampicin resistance (missense), and bacteriophage T6 resistance]. Tyrosine and, to a lesser extent, tryptophan (each at 2 mM) inhibited the mutagenicity of phenylalanine. Phenylalanine mutagenesis was detected in the uvrB strain, but not in the wild-type, uvrB umuC or uvrB lexA strains. Thus, phenylalanine seems to cause the production of excisable lesions ('UV-like'?) in DNA, which, if not excised, can induce mutations via error-prone DNA repair.
为了寻找一种可用于模拟正常代谢过程中产生的DNA损伤所诱导的“自发”突变的模型，研究人员在大肠杆菌K-12 uvrB中对19种氨基酸的致突变性进行了测试。结果发现，胱氨酸以及程度稍轻的精氨酸和苏氨酸具有抗诱变作用；只有苯丙氨酸具有诱变作用。在2 mM浓度下，苯丙氨酸诱导产生的突变体比背景水平高1.5至2倍[ lacZ53（琥珀突变）→Lac +、利福平抗性（错义突变）和噬菌体T6抗性]。酪氨酸以及程度稍轻的色氨酸（均为2 mM）可抑制苯丙氨酸的诱变作用。在uvrB菌株中检测到了苯丙氨酸诱变作用，但在野生型、uvrB umuC或uvrB lexA菌株中未检测到。因此，苯丙氨酸似乎会导致DNA中产生可切除的损伤（“类紫外线”损伤？），如果这些损伤未被切除，则可通过易错DNA修复诱导突变。
