Ruiz-Echevarría M J, de la Torre M A, Díaz-Orejas R
Centro de Investigaciones Biológicas, C.S.I.C., Madrid, Spain.
FEMS Microbiol Lett. 1995 Aug 1;130(2-3):129-35. doi: 10.1111/j.1574-6968.1995.tb07709.x.
The silent parD (kis/kid) stability operon of plasmid R1 is normally repressed by the co-ordinated action of the Kis and Kid proteins. In this report it is shown that a mutation in repA, the gene of the plasmid replication protein, that reduces two-fold the copy number of the plasmid, leads to the derepression of the parD system. This derepression can be prevented by a suppressor mutation in copB, a copy number control gene of plasmid R1, that increases the efficiency of replication of the repA mutant. Derepression of the wild-type parD system leads to high plasmid stability. These data show the activation of a plasmid stability operon by a mutation that reduces the efficiency of wild-type plasmid replication.
质粒R1的沉默parD（kis/kid）稳定性操纵子通常受到Kis和Kid蛋白协同作用的抑制。本报告表明，质粒复制蛋白基因repA中的一个突变使质粒拷贝数减少两倍，导致parD系统的去抑制。这种去抑制可通过质粒R1的拷贝数控制基因copB中的一个抑制突变来防止，该突变提高了repA突变体的复制效率。野生型parD系统的去抑制导致高质粒稳定性。这些数据表明，一个降低野生型质粒复制效率的突变激活了一个质粒稳定性操纵子。
