Denoya C D, Bechhofer D H, Dubnau D
J Bacteriol. 1986 Dec;168(3):1133-41. doi: 10.1128/jb.168.3.1133-1141.1986.
ermC specifies an rRNA methyltransferase that confers resistance to erythromycin. The expression of this determinant is induced by the addition of erythromycin. The induction mechanism has been shown to operate posttranscriptionally, and its mechanism has been elucidated. We now show that synthesis of the ermC gene product in Bacillus subtilis is also autoregulated by a mechanism operating on the level of translation. The synthesis of methyltransferase was shown to be gene dosage compensated by Western blot analysis. Several mutants were analyzed that specify altered ermC gene products and are deregulated. Analysis of mutants and of the wild-type strain by Northern blotting demonstrated that autoregulation is posttranscriptional. We suggest a translational repression model in which the ermC methyltransferase binds to its own mRNA, at a region that resembles the methylation target site on 23S rRNA. The overall control of ermC expression is discussed in light of these multiple regulatory mechanisms.
ermC基因编码一种赋予对红霉素耐药性的rRNA甲基转移酶。该决定簇的表达由添加红霉素诱导。已证明诱导机制在转录后起作用,且其机制已被阐明。我们现在表明,枯草芽孢杆菌中ermC基因产物的合成也通过一种在翻译水平上起作用的机制进行自我调节。通过蛋白质免疫印迹分析表明甲基转移酶的合成在基因剂量上得到补偿。分析了几个指定改变的ermC基因产物且不受调控的突变体。通过Northern印迹法对突变体和野生型菌株进行分析表明自我调节是转录后的。我们提出一种翻译抑制模型,其中ermC甲基转移酶在类似于23S rRNA上甲基化靶位点的区域与其自身mRNA结合。根据这些多种调控机制讨论了ermC表达的总体控制。