Bockrath R, Ruiz-Rubio M
Medical Research Council Cell Mutation Unit, University of Sussex, UK.
Mol Gen Genet. 1988 Oct;214(2):361-4. doi: 10.1007/BF00337737.
The numbers of tyrosine tRNA ochre suppressor mutations arising spontaneously or after UV irradiation in different strains of Escherichia coli K12 are considered. The DNA sequence change requisite for this type of mutation would be a transversion at a cytosine between two purines, where pyrimidine-pyrimidine photoproducts could not form. We find that UV mutagenesis does not produce these tyrosine tRNA ochre suppressor mutations. With lexA51 recA441 defective cells, the spontaneous yield of these mutations is elevated and UV irradiation produces a significant decrease in the numbers of this particular mutation. As explanation we suggest that the spontaneous appearance of these mutations reflects mutation at apurinic sites, the efficiency of which is elevated in lexA51 recA441 cells (with derepressed SOS functions and an activated form of RecA protein). The addition of UV damage in the DNA of these cells cannot further stimulate the positive functions that are required for the production of these mutations and are typically associated with UV mutagenesis (induction of SOS functions, activation of RecA protein and introduction of a targeting photoproduct) but apparently can have a negative effect on mutagenesis, hitherto not realized.
本文考虑了在不同大肠杆菌K12菌株中自发产生或紫外线照射后出现的酪氨酸tRNA赭石型抑制突变的数量。这种类型的突变所需的DNA序列变化将是两个嘌呤之间胞嘧啶的颠换，在此处不会形成嘧啶-嘧啶光产物。我们发现紫外线诱变不会产生这些酪氨酸tRNA赭石型抑制突变。对于lexA51 recA441缺陷型细胞，这些突变的自发产生率升高，而紫外线照射会使这种特定突变的数量显著减少。作为解释，我们认为这些突变的自发出现反映了无嘌呤位点的突变，其效率在lexA51 recA441细胞中有所提高（具有去抑制的SOS功能和活化形式的RecA蛋白）。在这些细胞的DNA中添加紫外线损伤不能进一步刺激产生这些突变所需的正向功能，这些功能通常与紫外线诱变相关（诱导SOS功能、激活RecA蛋白和引入靶向光产物），但显然可能对诱变产生负面影响，这一点迄今尚未被认识到。
