Bell Trevor W, Turner Rowan M, Merryman Amanda M, Joseph Juliana J, Gregory Steven T, O'Connor Michael
Division of Biology and Biomedical Systems, School of Science and Engineering, University of Missouri-Kansas City, Rm 306 Spencer Hall5007 Rockhill Rd., Kansas City, MO, 64110, USA.
Metropolitan Community College, Longview Campus, 500 SW Longview Rd., Lee's Summit, MO, 64081, USA.
Arch Microbiol. 2025 May 16;207(7):146. doi: 10.1007/s00203-025-04349-5.
The RsmG methyltransferase modifies G527 in bacterial 16S rRNA and its inactivation confers low level streptomycin resistance. In contrast, high level streptomycin resistance typically requires specific alterations in ribosomal protein uS12 or 16S rRNA. Here, we have asked if rsmG inactivation alters the phenotypes of any of a collection of randomly-generated Escherichia coli uS12 mutants. While several uS12 mutants show moderately increased resistance to streptomycin when rsmG is inactivated (MIC = 10-40 µg/ml), a uS12 R85H/rsmG-inactivated strain uniquely displays very high resistance (MIC > 1,024 µg/ml). Additional genetic selections showed that rsmG null mutations combined with specific alterations in uS12 can generate streptomycin-dependence, or pseudo-dependence, in addition to resistance. Moreover, growth of several of these mutants on high concentrations of streptomycin is conditional on rsmG inactivation. Thus, loss of mG527 methylation affects the streptomycin phenotypes of distinct uS12 mutants and identifies an additional route to high-level streptomycin resistance in bacteria.
RsmG甲基转移酶修饰细菌16S rRNA中的G527，其失活会赋予低水平链霉素抗性。相比之下，高水平链霉素抗性通常需要核糖体蛋白uS12或16S rRNA发生特定改变。在此，我们探讨了rsmG失活是否会改变一组随机产生的大肠杆菌uS12突变体的任何表型。虽然几个uS12突变体在rsmG失活时对链霉素的抗性适度增加（最低抑菌浓度为10 - 40μg/ml），但一个uS12 R85H/rsmG失活菌株独特地表现出非常高的抗性（最低抑菌浓度>1024μg/ml）。进一步的遗传筛选表明，rsmG缺失突变与uS12中的特定改变相结合，除了产生抗性外，还可导致链霉素依赖性或假依赖性。此外，这些突变体中的几个在高浓度链霉素上的生长取决于rsmG失活。因此，mG527甲基化的缺失影响了不同uS12突变体的链霉素表型，并确定了细菌中高水平链霉素抗性的另一条途径。
