Schmidt L, Inselburg J
J Bacteriol. 1982 Aug;151(2):845-54. doi: 10.1128/jb.151.2.845-854.1982.
A deletion mutant of the colicin E1-derived plasmid, pDMS6642, exhibited an approximately fourfold increase in copy number. We subsequently isolated hydroxylamine-induced mutants of that plasmid that had a further increase in copy number. Analysis of them suggests that the increased copy number of pDMS6642 is associated with transcriptional readthrough from a Tn3 transposon into the region of ColE1 containing information that influences plasmid replication. The hydroxylamine mutation in one copy number mutant appeared to increase the plasmid copy number by stimulating readthrough transcription from the Tn3 transposon into the ColE1 replication control region, whereas the other hydroxylamine mutation acts by another mechanism.
源自大肠杆菌素E1的质粒pDMS6642的一个缺失突变体，其拷贝数增加了约四倍。随后我们分离出了该质粒的羟胺诱导突变体，这些突变体的拷贝数进一步增加。对它们的分析表明，pDMS6642拷贝数的增加与从Tn3转座子到ColE1区域的转录通读有关，ColE1区域包含影响质粒复制的信息。一个拷贝数突变体中的羟胺突变似乎通过刺激从Tn3转座子到ColE1复制控制区域的通读转录来增加质粒拷贝数，而另一个羟胺突变则通过另一种机制起作用。
