Abeles A L, Austin S J
Laboratory of Chromosome Biology, BRI-Basic Research Program, NCI-Frederick Cancer Research Facility, MD 21701.
EMBO J. 1987 Oct;6(10):3185-9. doi: 10.1002/j.1460-2075.1987.tb02630.x.
Plasmids driven by the plasmid replication origin of bacteriophage P1 cannot be established in Escherichia coli strains that are defective for the DNA adenine methylase (dam). Using a composite plasmid that has two origins, we show that the P1 origin cannot function even in a plasmid that is already established in a dam strain. An in vitro replication system for the P1 origin was developed that uses as a substrate M13 replicative-form DNA containing the minimal P1 origin. The reaction mixture contains a crude extract of E. coli and purified P1 RepA protein. In addition to being RepA dependent, synthesis was shown to be dependent on methylation of the dam methylase-sensitive sites of the substrate DNA. As the P1 origin contains five such sites in a small region known to be critical for origin function, it can be concluded that methylation of these sites is a requirement for initiation. This suggests that the postreplicational methylation of the origin may control reinitiation and contribute to the accuracy of the highly stringent copy-number control of the origin in vivo.
由噬菌体P1的质粒复制起点驱动的质粒无法在DNA腺嘌呤甲基化酶(dam)有缺陷的大肠杆菌菌株中建立。使用具有两个起点的复合质粒,我们发现即使在已在dam菌株中建立的质粒中,P1起点也无法发挥作用。开发了一种用于P1起点的体外复制系统,该系统使用含有最小P1起点的M13复制型DNA作为底物。反应混合物包含大肠杆菌的粗提物和纯化的P1 RepA蛋白。除了依赖RepA外,合成还显示依赖于底物DNA的dam甲基化酶敏感位点的甲基化。由于P1起点在已知对起点功能至关重要的小区域中包含五个这样的位点,因此可以得出结论,这些位点的甲基化是起始的必要条件。这表明起点的复制后甲基化可能控制重新起始,并有助于体内起点高度严格的拷贝数控制的准确性。