Miller C A, Beaucage S L, Cohen S N
Department of Genetics, Stanford University School of Medicine, California 94305-5120.
Cell. 1990 Jul 13;62(1):127-33. doi: 10.1016/0092-8674(90)90246-b.
Previous work has shown that a cis-acting locus (termed par for partitioning) on the pSC101 plasmid accomplishes its stable inheritance in dividing cell populations. We report here that the DNA of pSC101 derivatives lacking the par region shows a decrease in overall superhelical density as compared with DNA of wild-type pSC101. Chemicals and bacterial mutations that reduce negative DNA supercoiling increase the rate of loss of par plasmids and convert normally stable plasmids that have minimal par region deletions into unstable replicons. topA gene mutations, which increase negative DNA supercoiling, reverse the instability of partition-defective plasmids that utilize the pSC101, p15A, F, or oriC replication systems. Our observations show that the extent of negative supercoiling of plasmid DNA has major effects on the plasmid's inheritance and suggest a mechanism by which the pSC101 par region may exert its stabilizing effects.
先前的研究表明，pSC101质粒上的一个顺式作用位点（称为par用于分配）在分裂细胞群体中实现其稳定遗传。我们在此报告，与野生型pSC101的DNA相比，缺乏par区域的pSC101衍生物的DNA总体超螺旋密度降低。降低负DNA超螺旋的化学物质和细菌突变会增加par质粒的丢失率，并将具有最小par区域缺失的正常稳定质粒转化为不稳定的复制子。增加负DNA超螺旋的topA基因突变可逆转利用pSC101、p15A、F或oriC复制系统的分配缺陷型质粒的不稳定性。我们的观察结果表明，质粒DNA的负超螺旋程度对质粒的遗传有重大影响，并提出了pSC101 par区域可能发挥其稳定作用的机制。
