Nandi Suparno, Dey Debayan, Srinivas Pooja, Dunham Christine M, Conn Graeme L
Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, United States.
Department of Chemistry, Emory University, Atlanta, GA 30322, United States.
Nucleic Acids Res. 2025 Jul 8;53(13). doi: 10.1093/nar/gkaf618.
Loss of ribosomal RNA (rRNA) modifications incorporated by the intrinsic methyltransferase TlyA results in reduced sensitivity to tuberactinomycin antibiotics such as capreomycin. However, how rRNA methylation alters drug binding, particularly at the distant but functionally more important site in 23S rRNA helix 69 (H69), is currently unknown. We determined high-resolution cryo-electron microscopy structures of the Mycolicibacterium smegmatis 70S ribosome with or without the two ribose 2'-O-methyl modifications incorporated by TlyA. In the unmodified ribosome, the tip of H69 adopts a more compact conformation, positioning two key nucleotides (A2137 and C2138) such that interactions with capreomycin would be lost and the binding pocket partially occluded. Methylation of 23S rRNA nucleotide C2144 promotes conformational changes that result in a more favorable positioning of C2138 and adoption of a more open conformation to enable capreomycin binding. Molecular dynamics simulations and H69 RNA helical analyses additionally reveal specific propagation of these changes from the site of modification to the H69 tip, allosterically reconfiguring the capreomycin binding site. Methylation of h44 also results in structural rearrangements at the H69-h44 interface to support maintenance of these changes that favor antibiotic binding. This work thus reveals the effect and regulation of distant rRNA methylation on ribosome-targeting antibiotic binding.
由内在甲基转移酶TlyA掺入的核糖体RNA(rRNA)修饰的缺失导致对结核放线菌素类抗生素(如卷曲霉素)的敏感性降低。然而,rRNA甲基化如何改变药物结合,特别是在23S rRNA螺旋69(H69)中距离较远但功能上更重要的位点,目前尚不清楚。我们确定了耻垢分枝杆菌70S核糖体在有或没有TlyA掺入的两种核糖2'-O-甲基修饰情况下的高分辨率冷冻电子显微镜结构。在未修饰的核糖体中,H69的末端采用更紧凑的构象,定位两个关键核苷酸(A2137和C2138),这样与卷曲霉素的相互作用将会丧失,并且结合口袋部分被封闭。23S rRNA核苷酸C2144的甲基化促进构象变化,导致C2138处于更有利的位置,并采用更开放的构象以实现卷曲霉素结合。分子动力学模拟和H69 RNA螺旋分析还揭示了这些变化从修饰位点到H69末端的特定传播,变构重新配置卷曲霉素结合位点。h44的甲基化还导致H69-h44界面处的结构重排,以支持维持这些有利于抗生素结合的变化。因此,这项工作揭示了远距离rRNA甲基化对靶向核糖体抗生素结合的影响和调控。