作者: N. Vazquez-Laslop , D. Klepacki , D. C. Mulhearn , H. Ramu , O. Krasnykh
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摘要: Specific nascent peptides in the ribosome exit tunnel can elicit translation arrest. Such stalling is used for regulation of expression some bacterial and eukaryotic genes. The sensitive to additional cellular cues, most commonly binding specific small-molecular-weight cofactors ribosome. role programmed arrest unknown. By analyzing peptide- antibiotic-dependent that controls inducible antibiotic resistance genes bacteria, we have found directly recognized as a part modulating signal. Even minute structural alterations preclude it from assisting stalling, indicating importance precise molecular interactions drug with One sensors monitor structure 23S rRNA residue C2610, whose mutation reduces efficiency stalling. These findings establish new paradigm cofactor which small molecule along peptide sequences composite provokes translation. A similar mechanism could be by sense variety metabolites.