DiNardo S, Voelkel K A, Sternglanz R, Reynolds A E, Wright A
Cell. 1982 Nov;31(1):43-51. doi: 10.1016/0092-8674(82)90403-2.
Escherichia coli deletion mutants lacking DNA topoisomerase I have been identified previously and shown to grow at a normal rate. We show that such strains grow normally only because of spontaneously arising mutations that compensate for the topoisomerase I defect. Several of these compensatory mutations have been found to map at or near the genes encoding DNA gyrase, gyrA and gyrB. DNA gyrase assays of crude extracts show that strains carrying the mutations have lower gyrase activity. Thus the mutations are in the gyrase structural genes or in nearby regulatory sequences. These results, in conjunction with DNA supercoiling measurements of others, indicate that in vivo DNA superhelicity is a result of a balance between topoisomerase I and gyrase activities. An excess of negative supercoils due to an absence of topoisomerase I is deleterious to the cell, but a moderate gyrase deficiency is not harmful.
此前已鉴定出缺乏DNA拓扑异构酶I的大肠杆菌缺失突变体，并表明其能以正常速率生长。我们发现，此类菌株能正常生长仅是因为自发产生了补偿拓扑异构酶I缺陷的突变。已发现其中一些补偿性突变位于编码DNA促旋酶的基因gyrA和gyrB处或其附近。粗提物的DNA促旋酶分析表明，携带这些突变的菌株具有较低的促旋酶活性。因此，这些突变存在于促旋酶结构基因或附近的调控序列中。这些结果，连同其他人对DNA超螺旋的测量结果，表明体内DNA超螺旋状态是拓扑异构酶I和促旋酶活性之间平衡的结果。由于缺乏拓扑异构酶I而导致的负超螺旋过多对细胞有害，但适度的促旋酶缺陷并无危害。
