Mutations in Ribosomal Protein RplA or Treatment with Ribosomal Acting Antibiotics Activates Production of Aminoglycoside Efflux Pump SmeYZ in Stenotrophomonas maltophilia.
Mutations in Ribosomal Protein RplA or Treatment with Ribosomal Acting Antibiotics Activates Production of Aminoglycoside Efflux Pump SmeYZ in Stenotrophomonas maltophilia.
复制标题
核糖体蛋白 RplA 突变或核糖体作用抗生素治疗可激活嗜麦芽寡养单胞菌中氨基糖苷外排泵 SmeYZ 的产生。
DOI：
10.1128/aac.01524-19
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发表时间：
2020
影响因子：
4.9
通讯作者：
Calvopiña K
中科院分区：
文献类型：
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作者：
Calvopiña K
嗜麦芽窄养单胞菌的氨基糖苷耐药是多因素的，但最重要的机制是SmeYZ外排系统的过量产生。通过研究实验室选择的突变体和临床分离株，我们发现对50S核糖体蛋白L1 （RplA）的损伤可激活SmeYZ的产生。我们还发现，庆大霉素和米诺环素，靶向核糖体，诱导smeyz的表达。这些发现解释了SmeYZ在内在和突变获得性氨基糖苷抗性中的作用。
Aminoglycoside resistance in Stenotrophomonas maltophilia is multifactorial, but the most significant mechanism is overproduction of the SmeYZ efflux system. By studying laboratory-selected mutants and clinical isolates, we show here that damage to the 50S ribosomal protein L1 (RplA) activates SmeYZ production. We also show that gentamicin and minocycline, which target the ribosome, induce expression ofsmeYZ. These findings explain the role of SmeYZ in both intrinsic and mutationally acquired aminoglycoside resistance.