Miller C A, Cohen S N
Department of Genetics, Stanford University School of Medicine, California 94305.
Mol Microbiol. 1993 Aug;9(4):695-702. doi: 10.1111/j.1365-2958.1993.tb01730.x.
The incompatibility that pSC101-derived plasmids express toward each other is mediated by directly repeated sequences (iterons) located near the plasmid's replication origin. We report here that the pSC101 par locus, which stabilizes plasmid inheritance in dividing cell populations and alters DNA superhelicity, can function as a cis-acting enhancer of incompatibility, which we show is determined jointly by the copy number of the plasmid and the number of iterons per copy. A single synthetic 32 bp iteron sequence carried by the pUC19 plasmid confers strong pSC101-specific incompatibility in the absence of any other pSC101 sites but requires the par locus to express strong incompatibility when carried by a lower-copy-number plasmid. We propose a model by which the par locus can enhance the apparently antagonistic processes of incompatibility and pSC101 DNA replication while concurrently facilitating plasmid distribution during cell division.
源自pSC101的质粒之间的不相容性是由位于质粒复制起点附近的直接重复序列(迭代子)介导的。我们在此报告,pSC101 par位点在分裂细胞群体中稳定质粒遗传并改变DNA超螺旋,可作为不相容性的顺式作用增强子,我们证明这是由质粒的拷贝数和每个拷贝的迭代子数量共同决定的。pUC19质粒携带的单个合成32 bp迭代子序列在没有任何其他pSC101位点的情况下赋予强烈的pSC101特异性不相容性,但当由低拷贝数质粒携带时,需要par位点来表达强烈的不相容性。我们提出了一个模型,通过该模型par位点可以增强明显相互拮抗的不相容性和pSC101 DNA复制过程,并同时促进细胞分裂期间的质粒分配。