Sedgwick S G
Proc Natl Acad Sci U S A. 1975 Jul;72(7):2753-7. doi: 10.1073/pnas.72.7.2753.
A hypothesis that ultraviolet-induced mutagenesis arises from the induction of an error-prone mode of postreplication repair that requires the exrA+ recA+ genotype has been tested with alkaline sucrose gradient centrifugation coupled with assays of fixation determined by loss of photoreversibility. The inhibitor of protein synthesis, chloramphenicol, added before irradiation, prevented a small amount of postreplication repair and completely eliminated mutation fixation in E. coli WP2s uvrA. However, chloramphenicol did not affect strand joining: (a) in uvrA bacteria allowed 20 min of growth between irradiation and antibiotic treatment; (b) in nonmutable uvrA exrA bacteria; and (c) in uvrA tif bacteria grown at 42 degrees for 70 min before irradiation. These observations indicate that an inducible product is involved in a fraction of postreplication repair and is responsible for induced mutagenesis.
一种假说认为，紫外线诱导的诱变源于诱导一种易错的复制后修复模式，这种模式需要exrA+ recA+基因型，该假说已通过碱性蔗糖梯度离心结合光可逆性丧失所确定的固定测定进行了检验。在照射前添加蛋白质合成抑制剂氯霉素，可阻止少量复制后修复，并完全消除大肠杆菌WP2s uvrA中的突变固定。然而，氯霉素并不影响链连接：(a) 在uvrA细菌中，在照射和抗生素处理之间允许生长20分钟；(b) 在不可突变的uvrA exrA细菌中；以及(c) 在uvrA tif细菌中，在照射前于42摄氏度生长70分钟。这些观察结果表明，一种可诱导产物参与了一部分复制后修复，并负责诱导诱变。
