Departamento de Bioquímica de la Nutrición, Instituto Superior de Investigaciones Biológicas (INSIBIO), Instituto de Química Biológica Dr. Bernabé Bloj, Tucumán, Argentina.
FEMS Microbiol Lett. 2010 Oct;311(2):185-92. doi: 10.1111/j.1574-6968.2010.02090.x. Epub 2010 Aug 23.
The SbmA protein is involved in the transport of MccB17-, MccJ25-, bleomycin- and proline-rich peptides into the Escherichia coli cytoplasm. sbmA gene homologues were found in a variety of bacteria. However, the physiological role of this protein still remains unknown. Previously, we found that a combination of sbmA and tolC mutations in Tn10-carrying E. coli K-12 strains results in hypersusceptibility to tetracycline. In this work, we studied sbmA expression in a tolC mutant background and observed an increased expression throughout growth. We ruled out the global transcriptional regulator RpoS and the small RNA micF as intermediates in this regulation. The tolC mutation induced the expression of other well-characterized strong σ(E) -dependent promoters in E. coli. We observed that the increase in σ(E) activity led to a greater sbmA expression, conversely eliminating σ(E) prevented expression of sbmA. We also observed that the sbmA upregulation in a tolC mutant context was abolished in an rpoE-null strain. These results suggest a σ(E) -dependent positive regulation on sbmA by the tolC mutation. We hypothesize that this mechanism might be part of a compensatory cell envelope stress response.
SbmA 蛋白参与将 MccB17-、MccJ25-、博来霉素和富含脯氨酸的肽类物质运输到大肠杆菌细胞质中。在各种细菌中都发现了 sbmA 基因同源物。然而，该蛋白的生理作用仍然未知。先前，我们发现 Tn10 携带的大肠杆菌 K-12 菌株中 sbmA 和 tolC 突变的组合导致对四环素的敏感性增加。在这项工作中，我们研究了 tolC 突变背景下 sbmA 的表达情况，并观察到整个生长过程中表达增加。我们排除了全局转录调节剂 RpoS 和小分子 RNA micF 作为这种调节的中间物。tolC 突变诱导了大肠杆菌中其他特征明确的强 σ(E)依赖性启动子的表达。我们观察到 σ(E)活性的增加导致 sbmA 的表达增加，相反，消除 σ(E)则阻止了 sbmA 的表达。我们还观察到，在 tolC 突变背景下 sbmA 的上调在 rpoE 缺失菌株中被消除。这些结果表明 tolC 突变对 sbmA 进行了 σ(E)依赖性的正调控。我们假设这种机制可能是细胞包膜应激反应的一部分。
