Bridges B A, Sedgwick S G
J Bacteriol. 1974 Mar;117(3):1077-81. doi: 10.1128/jb.117.3.1077-1081.1974.
Daughter-strand gaps in deoxyribonucleic acid (DNA) synthesized after exposure of excision-deficient Escherichia coli to ultraviolet light are filled during subsequent incubation in buffer, and the rate of filling is increased when the incubation in buffer is carried out in the presence of 360-nm light. It is concluded that daughter-strand discontinuities are prevented from being rapidly sealed in the dark not because of some structural feature of the daughter-strand but because of the presence of a pyrimidine dimer on the opposite (parental) strand. "Photoreactivation-stimulated gap filling" is dependent on the polA(+) and recA(+) but not the exrA(+) genes. It is suggested that the removal of the dimer allows gap-filling by DNA polymerase I and polynucleotide ligase. The recA(+) gene may be needed at a very early stage, possibly for gap stabilization.
切除缺陷型大肠杆菌暴露于紫外线下后合成的脱氧核糖核酸(DNA)中的子代链缺口,在随后于缓冲液中孵育期间会被填补,并且当在360纳米光照存在下于缓冲液中孵育时,填补速率会增加。得出的结论是,子代链的间断在黑暗中不会迅速封闭,不是因为子代链的某些结构特征,而是因为相对(亲代)链上存在嘧啶二聚体。“光复活刺激的缺口填补”依赖于polA(+)和recA(+)基因,但不依赖于exrA(+)基因。有人提出,二聚体的去除允许DNA聚合酶I和多核苷酸连接酶进行缺口填补。recA(+)基因可能在非常早期阶段就需要,可能用于缺口稳定。