Almutairi Mashal M, Svetlov Maxim S, Hansen Douglas A, Khabibullina Nelli F, Klepacki Dorota, Kang Han-Young, Sherman David H, Vázquez-Laslop Nora, Polikanov Yury S, Mankin Alexander S
Center for Biomolecular Sciences, University of Illinois, Chicago, IL 60607, USA.
Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA.
Nucleic Acids Res. 2017 Sep 19;45(16):9573-9582. doi: 10.1093/nar/gkx673.
Antibiotics methymycin (MTM) and pikromycin (PKM), co-produced by Streptomyces venezuelae, represent minimalist macrolide protein synthesis inhibitors. Unlike other macrolides, which carry several side chains, a single desosamine sugar is attached to the macrolactone ring of MTM and PKM. In addition, the macrolactone scaffold of MTM is smaller than in other macrolides. The unusual structure of MTM and PKM and their simultaneous secretion by S. venezuelae bring about the possibility that two compounds would bind to distinct ribosomal sites. However, by combining genetic, biochemical and crystallographic studies, we demonstrate that MTM and PKM inhibit translation by binding to overlapping sites in the ribosomal exit tunnel. Strikingly, while MTM and PKM readily arrest the growth of bacteria, ∼40% of cellular proteins continue to be synthesized even at saturating concentrations of the drugs. Gel electrophoretic analysis shows that compared to other ribosomal antibiotics, MTM and PKM prevent synthesis of a smaller number of cellular polypeptides illustrating a unique mode of action of these antibiotics.
委内瑞拉链霉菌共同产生的抗生素美他霉素(MTM)和苦霉素(PKM)是极简主义大环内酯类蛋白质合成抑制剂。与其他带有多个侧链的大环内酯类不同,MTM和PKM的大环内酯环上仅连接有一个去氧胺糖。此外,MTM的大环内酯支架比其他大环内酯类更小。MTM和PKM的独特结构以及它们由委内瑞拉链霉菌同时分泌,使得这两种化合物可能结合到不同的核糖体位点。然而,通过结合遗传学、生物化学和晶体学研究,我们证明MTM和PKM通过结合核糖体出口通道中的重叠位点来抑制翻译。令人惊讶的是,虽然MTM和PKM能轻易地阻止细菌生长,但即使在药物饱和浓度下,仍有~40%的细胞蛋白质继续合成。凝胶电泳分析表明,与其他核糖体抗生素相比,MTM和PKM阻止合成的细胞多肽数量更少,说明了这些抗生素独特的作用方式。