Bravo A, Ortega S, de Torrontegui G, Díaz R
Centro de Investigaciones Biológicas, (C.S.I.C.), Madrid, Spain.
Mol Gen Genet. 1988 Dec;215(1):146-51. doi: 10.1007/BF00331316.
The proteins P10 and P12 have been shown to be gene products of a new stability system, ParD, of plasmid R1. It is now shown that an R1 miniplasmid, pAB112, carrying a trans-complementable amber mutation in the gene of the P10 protein, is lethal for the host in the absence of suppression. This lethal effect is suppressed in a supF background and also by deletions in pAB112 that affect the gene of the P12 protein. These data indicate that the P12 protein has a lethal effect on the host and that this effect is neutralized by the P10 protein. The possibility that the stabilization conferred by the ParD system could be due to a counterselection, mediated by P12, of cells that lose the plasmid at cell division, is discussed.
蛋白质P10和P12已被证明是质粒R1新的稳定性系统ParD的基因产物。现在发现,携带P10蛋白基因中可反式互补琥珀突变的R1微型质粒pAB112,在没有抑制作用的情况下对宿主是致死的。这种致死效应在supF背景中以及通过影响P12蛋白基因的pAB112缺失得到抑制。这些数据表明,P12蛋白对宿主有致死作用,而这种作用被P10蛋白中和。文中讨论了ParD系统赋予的稳定性可能是由于P12介导的对在细胞分裂时丢失质粒的细胞进行反选择的可能性。