Bockrath R, Li B H
Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis 46202-5120, USA.
Mol Gen Genet. 1995 Dec 20;249(6):591-9. doi: 10.1007/BF00418028.
Mutation frequency decline (MFD) in Escherichia coli was examined to demonstrate repair of targeting photoproducts during the post-UV incubation required in this process. Repair of mutation-targeting cyclobutane pyrimidine dimers (T < > C) was demonstrated when a correlation was established between the mutation frequency normally associated with these lesions and the rate of mutation production at these lesions by spontaneous deamination of cytosines and photoreversal in ung-defective cells. An incubation producing a decline in mutation frequency, i.e., MFD, also produces lower rates of mutation increase via the deamination mechanism. Since the latter assay involves processes entirely within the post-UV incubation period, the lower rates are attributed to rapid transcription-coupled nucleotide excision repair (TCR) that reduces the number of relevant T < > C dimers during this period. Rediscovery of the neglected fact that MFD can be stimulated by post-UV incubation in buffer alone is part of the analysis. Results presented here and a variety of others are discussed to support a model of MFD as a particular example of TCR: effective repair of photoproducts in the transcribed DNA strand that target glutamine tRNA suppressor mutations occurs during the appropriate post-UV incubation and is responsible for MFD.
对大肠杆菌中的突变频率下降（MFD）进行了检测，以证明在此过程所需的紫外线照射后孵育期间靶向光产物的修复情况。当在正常与这些损伤相关的突变频率与无尿嘧啶-DNA糖基化酶缺陷细胞中胞嘧啶自发脱氨基和光逆转导致的这些损伤处的突变产生速率之间建立相关性时，证明了靶向突变的环丁烷嘧啶二聚体（T<>C）的修复。产生突变频率下降（即MFD）的孵育也会通过脱氨基机制产生较低的突变增加速率。由于后一种检测方法涉及的过程完全在紫外线照射后的孵育期内，较低的速率归因于快速转录偶联核苷酸切除修复（TCR），该修复在此期间减少了相关T<>C二聚体的数量。重新发现被忽视的事实，即仅在缓冲液中进行紫外线照射后孵育就可以刺激MFD，这是分析的一部分。本文给出的结果和其他各种结果进行了讨论，以支持将MFD作为TCR的一个具体例子的模型：在适当的紫外线照射后孵育期间，靶向谷氨酰胺tRNA抑制基因突变的转录DNA链中的光产物得到有效修复，这就是MFD的原因。
