Gross Christian H, Parsons Jonathan D, Grossman Trudy H, Charifson Paul S, Bellon Steven, Jernee James, Dwyer Maureen, Chambers Stephen P, Markland William, Botfield Martyn, Raybuck Scott A
Vertex Pharmaceuticals Incorporated, Cambridge, Massachusetts 02139, USA.
Antimicrob Agents Chemother. 2003 Mar;47(3):1037-46. doi: 10.1128/AAC.47.3.1037-1046.2003.
DNA gyrase is a bacterial type II topoisomerase which couples the free energy of ATP hydrolysis to the introduction of negative supercoils into DNA. Amino acids in proximity to bound nonhydrolyzable ATP analog (AMP. PNP) or novobiocin in the gyrase B (GyrB) subunit crystal structures were examined for their roles in enzyme function and novobiocin resistance by site-directed mutagenesis. Purified Escherichia coli GyrB mutant proteins were complexed with the gyrase A subunit to form the functional A(2)B(2) gyrase enzyme. Mutant proteins with alanine substitutions at residues E42, N46, E50, D73, R76, G77, and I78 had reduced or no detectable ATPase activity, indicating a role for these residues in ATP hydrolysis. Interestingly, GyrB proteins with P79A and K103A substitutions retained significant levels of ATPase activity yet demonstrated no DNA supercoiling activity, even with 40-fold more enzyme than the wild-type enzyme, suggesting that these amino acid side chains have a role in the coupling of the two activities. All enzymes relaxed supercoiled DNA to the same extent as the wild-type enzyme did, implying that only ATP-dependent reactions were affected. Mutant genes were examined in vivo for their abilities to complement a temperature-sensitive E. coli gyrB mutant, and the activities correlated well with the in vitro activities. We show that the known R136 novobiocin resistance mutations bestow a significant loss of inhibitor potency in the ATPase assay. Four new residues (D73, G77, I78, and T165) that, when changed to the appropriate amino acid, result in both significant levels of novobiocin resistance and maintain in vivo function were identified in E. coli.
DNA促旋酶是一种细菌II型拓扑异构酶,它将ATP水解的自由能与向DNA中引入负超螺旋偶联起来。通过定点诱变,研究了促旋酶B(GyrB)亚基晶体结构中靠近结合的不可水解ATP类似物(AMP.PNP)或新生霉素的氨基酸在酶功能和新生霉素抗性中的作用。纯化的大肠杆菌GyrB突变蛋白与促旋酶A亚基复合,形成功能性A(2)B(2)促旋酶。在E42、N46、E50、D73、R76、G77和I78残基处被丙氨酸取代的突变蛋白具有降低的或不可检测的ATP酶活性,表明这些残基在ATP水解中起作用。有趣的是,具有P79A和K103A取代的GyrB蛋白保留了显著水平的ATP酶活性,但即使酶量比野生型酶多40倍,也没有表现出DNA超螺旋活性,这表明这些氨基酸侧链在两种活性的偶联中起作用。所有酶将超螺旋DNA松弛到与野生型酶相同的程度,这意味着只有ATP依赖性反应受到影响。在体内检测突变基因对温度敏感的大肠杆菌gyrB突变体的互补能力,其活性与体外活性相关性良好。我们表明,已知的R136新生霉素抗性突变在ATP酶测定中导致抑制剂效力显著丧失。在大肠杆菌中鉴定出四个新的残基(D73、G77、I78和T165),当它们被改变为合适的氨基酸时,会导致显著水平的新生霉素抗性并维持体内功能。