Center for Advanced Biotechnology and Medicine, Piscataway, NJ 08854, USA.
Curr Opin Struct Biol. 2009 Dec;19(6):715-23. doi: 10.1016/j.sbi.2009.10.010. Epub 2009 Nov 18.
Inhibition of bacterial RNA polymerase (RNAP) is an established strategy for antituberculosis therapy and broad-spectrum antibacterial therapy. Crystal structures of RNAP-inhibitor complexes are available for four classes of antibiotics: rifamycins, sorangicin, streptolydigin, and myxopyronin. The structures define three different targets, and three different mechanisms, for inhibition of bacterial RNAP: (1) rifamycins and sorangicin bind near the RNAP active center and block extension of RNA products; (2) streptolydigin interacts with a target that overlaps the RNAP active center and inhibits conformational cycling of the RNAP active center; and (3) myxopyronin interacts with a target remote from the RNAP active center and functions by interfering with opening of the RNAP active-center cleft to permit entry and unwinding of DNA and/or by interfering with interactions between RNAP and the DNA template strand. The structures enable construction of homology models of pathogen RNAP-antibiotic complexes, enable in silico screening for new antibacterial agents, and enable rational design of improved antibacterial agents.
抑制细菌 RNA 聚合酶(RNAP)是抗结核治疗和广谱抗菌治疗的一种既定策略。有四类抗生素的 RNAP-抑制剂复合物的晶体结构:利福霉素类、索拉菌素、链霉溶菌素和粘菌素。这些结构定义了抑制细菌 RNAP 的三种不同的靶标和三种不同的机制:(1)利福霉素类和索拉菌素结合在 RNAP 活性中心附近,阻止 RNA 产物的延伸;(2)链霉溶菌素与重叠 RNAP 活性中心的靶标相互作用,抑制 RNAP 活性中心的构象循环;(3)粘菌素与远离 RNAP 活性中心的靶标相互作用,通过干扰 RNAP 活性中心裂隙的打开来干扰 DNA 的进入和解旋,以及/或干扰 RNAP 与 DNA 模板链之间的相互作用,从而发挥作用。这些结构使我们能够构建病原体 RNAP-抗生素复合物的同源模型,能够进行新的抗菌药物的计算机筛选,并能够合理设计改进的抗菌药物。