The Expression of Antibiotic Resistance Methyltransferase Correlates with mRNA Stability Independently of Ribosome Stalling

摘要: Members of the Erm methyltransferase family modify 23S rRNA bacterial ribosome and render cross-resistance to macrolides multiple distantly related antibiotics. Previous studies have shown that expression erm is activated when a macrolide-bound stalls translation leader peptide preceding cotranscribed Ribosome stalling thought destabilize inhibitory stem-loop mRNA structure exposes Shine-Dalgarno (SD) sequence for translational initiation. Paradoxically, mutations abolish are routinely found in hyper-resistant clinical isolates; however, significance stalling-dead largely unknown. Here, we show nonsense Staphylococcus aureus ErmB (ErmBL) lead high basal induced downstream absence or presence macrolide concomitantly with elevated methylation resistance. The overexpression associated reduced turnover ermBL-ermB transcript, appears mitigate cleavage at site immediately ermBL SD sequence. stabilizing effect antibiotics on not limited ermBL-ermB; cationic representing ribosome-stalling inducer noninducer increase half-life specific transcripts. These data unveil new layer ermB regulation imply ErmBL serves as "tuner" suppress aberrant production because methylated may impose fitness cost bacterium result misregulated translation.