Grundström T, Normark S
Mol Gen Genet. 1985;198(3):411-5. doi: 10.1007/BF00332931.
The chromosomal beta-lactamase gene of E. coli, ampC, shows increased expression with increased growth rate of the bacteria. We have previously shown that transcription of ampC is attenuated, and that a mutation in the terminator stem of this attenuator abolishes the growth rate-dependency of ampC expression. We now present studies using mutations, made in vitro, located such that the 5'-end of ampC mRNA carries a possible recognition sequence for initiation of translation close to the attenuator stem. Alteration of the supposed initiation codon AUG to UUG resulted in a reduced and growth rate-independent expression of ampC beta-lactamase. AmpC mRNA starts with the sequence AUC, which might be a non-typical ribosome binding site, situated four bases before the AUG. Deletion of the C in this sequence caused a partial reduction of ampC expression and also a partial loss of the growth rate-dependent regulation. The phenotypes of these mutants support a model in which formation of a ribosome initiation complex at a level increasing with the growth rate inhibits termination of transcription at the ampC attenuator.
大肠杆菌的染色体β-内酰胺酶基因ampC随着细菌生长速率的增加而表达增强。我们之前已经表明ampC的转录会受到衰减,并且该衰减子终止茎中的突变会消除ampC表达对生长速率的依赖性。我们现在展示了使用体外构建的突变进行的研究,这些突变的位置使得ampC mRNA的5'端在靠近衰减子茎的位置带有一个可能用于翻译起始的识别序列。将假定的起始密码子AUG改变为UUG导致ampCβ-内酰胺酶的表达降低且与生长速率无关。AmpC mRNA以序列AUC起始,这可能是一个非典型的核糖体结合位点,位于AUG之前四个碱基处。该序列中C的缺失导致ampC表达部分降低,同时也部分丧失了生长速率依赖性调控。这些突变体的表型支持一种模型,即核糖体起始复合物在随着生长速率增加的水平上形成会抑制ampC衰减子处的转录终止。