Takeya T, Shimada K, Oka A, Takagi Y
J Bacteriol. 1979 Oct;140(1):294-6. doi: 10.1128/jb.140.1.294-296.1979.
The plaque-forming ability of a hybrid phage between plasmidColE1 and phage lambda carrying amber mutations in genes O and P was inhibited by the presence of ColE1 in suppressor-deficient Escherichia coli cells. ColE1 deoxyribonucleic acid regions concerned with this inhibition were examined by using various deletion and transposon insertion derivatives of ColE1, and it was found that the presence of the deoxyribonucleic acid region extending between 420 and 613 base pairs upstream from the initiation site of ColE1 deoxyribonucleic acid replication (J. Tomizawa, H. Ohmori, and R. E. Bird, Proc. Natl. Acad. Sci. U. S. A. 74: 1865--1869, 1977) was essential for this function.
在缺乏抑制因子的大肠杆菌细胞中,携带琥珀突变的基因O和P的质粒ColE1与噬菌体λ之间的杂交噬菌体的噬菌斑形成能力受到ColE1的抑制。通过使用ColE1的各种缺失和转座子插入衍生物,研究了与这种抑制作用相关的ColE1脱氧核糖核酸区域,发现从ColE1脱氧核糖核酸复制起始位点上游420至613个碱基对之间延伸的脱氧核糖核酸区域的存在对该功能至关重要(J. 富泽、大森博史和R. E. 伯德,《美国国家科学院院刊》74: 1865 - 1869, 1977)。