Mattes R, Burkardt H J, Schmitt R
Mol Gen Genet. 1979 Jan 10;168(2):173-84. doi: 10.1007/BF00431443.
The 30 megadalton (Mdal)-conjugative, fi- plasmid pRSD1 determines inducible tetracycline resistance (Tc) in Escherichia coli. As shown by restriction analysis, a 3.5 Mdal-EcoRI fragment of pRSD1 spliced into the small plasmid pRSD2124 comprises the entire Tc determinant (tet) region. A restriction map of pRSD1 is presented which includes the location of the tet region and of an "underwound" loop not related to Tc (Burkardt et al., 1978). Selective amplification of tet genes is demonstrated by three lines of evidence. (i) The resistance level of cell harbouring pRSD1 increases approximately tenfold by induction with 10 microgram/ml of tetracycline. Further growth in the presence of 100 microgram/ml of the drug ("tetracycline stress") selects for cells with even higher resistance levels (about 300 microgram/ml) in rec+ cells. In a recA strain, a smaller proportion of cells attains these high resistance levels suggesting the involvement of host recombination. (ii) Electron micrographs of pRSD1-DNA isolated from tetracycline-stressed cells reveal a heterogeneous population of circular DNA molecules ranging between 1.7 and 21.6 micron. The distribution of contour lengths shows a discrete pattern ascribed to the presence of autonomous single- and multiple-copy Tc determinants and to intact plasmids containing zero to six tet regions in tandem repeats. (iii) This interpretation is supported by heteroduplex and restriction analyses which demonstrate the presence of multiple copies of the 3.5 Mdal-element encompassing the tet region in pRSD1 molecules selected by tetracycline stress. It has been concluded that gene amplification leading to tandem repetition of the tet region ensues in pRSD1. Such plasmids confer increased tetracycline resistance and can, thefore, be selected by high doses of the drug.
30兆道尔顿(Mdal)的接合型F1质粒pRSD1可决定大肠杆菌中可诱导的四环素抗性(Tc)。如限制性酶切分析所示,pRSD1的一个3.5 Mdal - EcoRI片段拼接至小质粒pRSD2124中,包含了整个四环素决定簇(tet)区域。本文给出了pRSD1的限制性酶切图谱,其中包括tet区域以及与四环素抗性无关的“解旋”环的位置(Burkardt等人,1978年)。三条证据表明存在tet基因的选择性扩增。(i)携带pRSD1的细胞在10微克/毫升四环素诱导下,抗性水平大约增加10倍。在100微克/毫升药物(“四环素胁迫”)存在的情况下进一步生长,可筛选出rec⁺细胞中具有更高抗性水平(约300微克/毫升)的细胞。在recA菌株中,达到这些高抗性水平的细胞比例较小,这表明宿主重组参与其中。(ii)从四环素胁迫细胞中分离出的pRSD1 - DNA的电子显微镜照片显示,环状DNA分子群体具有异质性,长度在1.7至21.6微米之间。轮廓长度的分布呈现出离散模式,这归因于自主单拷贝和多拷贝四环素决定簇的存在,以及含有零至六个tet区域串联重复的完整质粒。(iii)异源双链体和限制性酶切分析支持了这一解释,这些分析表明在四环素胁迫选择的pRSD1分子中,存在包含tet区域的3.5 Mdal元件的多个拷贝。得出的结论是,pRSD1中会发生导致tet区域串联重复的基因扩增。此类质粒赋予更高的四环素抗性,因此可通过高剂量药物进行筛选。