Makino F, Munakata N
J Bacteriol. 1978 Apr;134(1):24-9. doi: 10.1128/jb.134.1.24-29.1978.
DNA extracted from exponentially growing cells of thymine-requiring Bacillus subtilis strains with defective N-glycosidase activity for deoxyuridine residues in DNA was subjected to the action of N-glycosidase in vitro and analyzed by sedimentation in alkaline sucrose gradients. The sites attacked by N-glycosidase occurred once per 6 X 10(6) to 7 X 10(6) daltons of DNA from cells cultured in the presence of growth-supporting concentrations of thymine. The number of N-glycosidase-susceptible sites increased when the thymine concentration in the medium was lowered. Parallel to this observation, the N-glycosidase-defective mutant cells were less apt to show the detrimental effect due to thymine depletion than were the parental cells. Such sites were not detected in DNA from cells with a normal N-glycosidase activity or with a "wild type" capacity for thymidylate synthesis. The results are interpreted to mean that cells defective for thymidylate synthesis incorporate dUTP in place of TTP in DNA and that the deoxyuridine residues, once incorporated, remain in the DNA in the absence of N-glycosidase activity.
从需要胸腺嘧啶的枯草芽孢杆菌菌株中提取DNA,这些菌株的N-糖苷酶活性对于DNA中的脱氧尿苷残基存在缺陷,提取的DNA在体外经N-糖苷酶作用后,通过碱性蔗糖梯度沉降进行分析。在含有支持生长浓度胸腺嘧啶的条件下培养的细胞中,每6×10⁶至7×10⁶道尔顿的DNA中,N-糖苷酶攻击的位点出现一次。当培养基中胸腺嘧啶浓度降低时,N-糖苷酶敏感位点的数量增加。与此观察结果平行的是,与亲本细胞相比,N-糖苷酶缺陷型突变细胞因胸腺嘧啶耗尽而显示出有害作用的可能性较小。在具有正常N-糖苷酶活性或具有胸苷酸合成“野生型”能力的细胞的DNA中未检测到此类位点。结果被解释为意味着胸苷酸合成缺陷的细胞在DNA中掺入dUTP以取代TTP,并且一旦掺入,脱氧尿苷残基在没有N-糖苷酶活性的情况下会保留在DNA中。