Pons F W, Müller P
Institut für Mikrobiologie, J.W. Goethe-Universität, Frankfurt-am-Main, F.R.G.
Mutat Res. 1989 Jan;210(1):71-7. doi: 10.1016/0027-5107(89)90046-8.
Log-phase cells of E. coli growing in defined minimal media were washed, exposed to acridines in the same minimal salts solution, and plated to select for Nad+ revertants. At low mutagen concentration, treatment in the presence of the carbon source to which the cells were adapted resulted in a decrease in revertant yield of several orders of magnitude compared with the yield in the absence of a carbon source. At high mutagen concentration, however, a carbon source present during treatment caused a 2- to 150-fold increase in revertant yield (depending on the mutagen, the carbon source, and on the genetic background of the strain). In a strain lacking adenylate cyclase, acridine mutagenesis was not abolished under the experimental conditions used in this study, and the addition of cAMP during mutagenic treatment had no effect. In mismatch repair-deficient strains, the presence of glucose during treatment with low mutagen concentration did not cause a decrease in revertant yield as drastic as in the wild type. From the results reported here, we conclude that the glucose effect in acridine mutagenesis is due to an enhancement of mismatch repair.
在限定的基本培养基中生长的大肠杆菌对数期细胞被洗涤后，在相同的基本盐溶液中暴露于吖啶类化合物，然后进行平板接种以筛选Nad +回复突变体。在低诱变剂浓度下，在细胞适应的碳源存在下进行处理，与无碳源时相比，回复突变体产量降低了几个数量级。然而，在高诱变剂浓度下，处理期间存在的碳源使回复突变体产量增加了2至150倍（取决于诱变剂、碳源和菌株的遗传背景）。在缺乏腺苷酸环化酶的菌株中，在本研究使用的实验条件下，吖啶诱变并未被消除，并且在诱变处理期间添加cAMP没有效果。在错配修复缺陷型菌株中，低诱变剂浓度处理期间葡萄糖的存在不会像野生型那样导致回复突变体产量急剧下降。根据此处报道的结果，我们得出结论，吖啶诱变中的葡萄糖效应是由于错配修复的增强。
