Fukuda M, Shimizu S, Okita N, Seto M, Masai E
Department of Bioengineering, Nagaoka University of Technology, Niigata, Japan.
Antonie Van Leeuwenhoek. 1998 Jul-Oct;74(1-3):169-73. doi: 10.1023/a:1001732718159.
Polychlorinated biphenyl (PCB) tolerant derivatives of a strong PCB degrader, Rhodococcus strain RHA1, were selected after growth in the presence of 100 micrograms/ml PCBs. Some of the derivatives did not grow on biphenyl but accumulated a yellow coloured metabolite suggesting a defect in the meta-ring-cleavage compound hydrolase step encoded by the bphD gene. Other derivatives failed to grow on biphenyl and exhibited little PCB transformation activity suggesting a defect in the initial ring-hydroxylation dioxygenase step encoded by the bphA gene. These organisms had a structural alteration in the linear plasmids coding for the bph genes in RHA1, which included the bph gene deletion. When a bphD containing plasmid was introduced into a tolerant derivative, RCD1, which was shown to have bphD deletion, the defect in the growth on biphenyl of RCD1 was overcome. The bph gene deletion seems to play a key role in these tolerant derivatives thereby suggesting that the toxic metabolic intermediate would be a main cause of the growth inhibition of RHA1 in the presence of high concentration PCBs.
在含有100微克/毫升多氯联苯（PCB）的环境中培养后，筛选出了强PCB降解菌红球菌RHA1的耐PCB衍生物。一些衍生物不能在联苯上生长，但积累了一种黄色代谢物，这表明由bphD基因编码的间位环裂解化合物水解酶步骤存在缺陷。其他衍生物不能在联苯上生长，并且几乎没有PCB转化活性，这表明由bphA基因编码的初始环羟基化双加氧酶步骤存在缺陷。这些生物体在编码RHA1中bph基因的线性质粒上发生了结构改变，其中包括bph基因缺失。当将含有bphD的质粒导入已证明存在bphD缺失的耐PCB衍生物RCD1中时，RCD1在联苯上生长的缺陷得以克服。bph基因缺失似乎在这些耐PCB衍生物中起关键作用，从而表明有毒代谢中间体可能是高浓度PCB存在下RHA1生长受抑制的主要原因。
