Schäferjohann J, Bednarski R, Bowien B
Institut für Mikrobiologie, Georg-August-Universität Göttingen, Germany.
J Bacteriol. 1996 Dec;178(23):6714-9. doi: 10.1128/jb.178.23.6714-6719.1996.
In the facultatively chemoautotrophic bacterium Ralstonia eutropha (formerly Alcaligenes eutrophus), most genes required for CO2 assimilation via the Calvin cycle are organized within two highly homologous cbb operons located on the chromosome and on megaplasmid pHG1, respectively, of strain H16. These operons are subject to tight control exerted by a promoter upstream of the 5'-terminal cbbL gene that is regulated by the activator CbbR. The existence of subpromoters within the operons was now excluded, as determined with lacZ operon fusions to suitable cbb gene fragments in the promoter-probe vector pBK. Nevertheless, marked differential expression of the promoter-proximal ribulose-1,5-bisphosphate carboxylase-oxygenase genes cbbLS and the remaining distal genes occurs within the operons. Computer analysis revealed a potential stem-loop structure immediately downstream of cbbS that was suspected to be involved in the differential gene expression. Nuclease S1 mapping identified a major 3' end and a minor 3' end of the relatively stable cbbLS partial transcript just downstream of this structure. Moreover, operon fusions containing progressively deleted stem-loop structures showed that the structure primarily caused transcriptional termination downstream of cbbS rather than increased the segmental stability of the cbbLS transcript. Premature transcription termination thus represents an important mechanism leading to differential gene expression within the cbb operons.
在兼性化学自养细菌罗尔斯通氏真养菌(以前称为食酸菌真养菌)中,通过卡尔文循环同化二氧化碳所需的大多数基因分别位于菌株H16染色体和大质粒pHG1上的两个高度同源的cbb操纵子内。这些操纵子受到由激活剂CbbR调控的5'-末端cbbL基因上游启动子的严格控制。如用启动子探针载体pBK中合适的cbb基因片段与lacZ操纵子融合所确定的那样,现在已排除操纵子内存在亚启动子。然而,操纵子近端的1,5-二磷酸核酮糖羧化酶-加氧酶基因cbbLS与其余远端基因之间存在明显的差异表达。计算机分析揭示了cbbS下游紧邻处有一个潜在的茎环结构,怀疑其与差异基因表达有关。核酸酶S1图谱分析确定了该结构下游相对稳定的cbbLS部分转录本的一个主要3'末端和一个次要3'末端。此外,含有逐步缺失的茎环结构的操纵子融合表明,该结构主要导致cbbS下游的转录终止,而不是增加cbbLS转录本的片段稳定性。因此,过早的转录终止是导致cbb操纵子内差异基因表达的一个重要机制。