Department of Microbial Infection and Immunity, Ohio State University, Columbus, OH, USA.
J Bacteriol. 2013 Apr;195(8):1637-44. doi: 10.1128/JB.02190-12. Epub 2013 Jan 25.
Pseudomonas aeruginosa strains recovered from chronic pulmonary infections in cystic fibrosis patients are frequently mucoid. Such strains express elevated levels of alginate but reduced levels of the aggregative polysaccharide Psl; however, the mechanistic basis for this regulation is not completely understood. Elevated pslA expression was observed in an amrZ null mutant and in strains expressing a DNA-binding-deficient AmrZ. AmrZ is a transcription factor that positively regulates twitching motility and alginate synthesis, two phenotypes involved in P. aeruginosa biofilm development. AmrZ bound directly to the pslA promoter in vitro, and molecular analyses indicate that AmrZ represses psl expression by binding to a site overlapping the promoter. Altered expression of amrZ in nonmucoid strains impacted biofilm structure and architecture, as structured microcolonies were observed with low AmrZ production and flat biofilms with amrZ overexpression. These biofilm phenotypes correlated with Psl levels, since we observed elevated Psl production in amrZ mutants and lower Psl production in amrZ-overexpressing strains. These observations support the hypothesis that AmrZ is a multifunctional regulator mediating transition of P. aeruginosa biofilm infections from colonizing to chronic biofilms through repression of the psl operon while activating the algD operon.
铜绿假单胞菌菌株从囊性纤维化患者的慢性肺部感染中恢复，经常是粘液型的。这种菌株表达高水平的藻酸盐，但聚集多糖 Psl 的水平降低;然而，这种调节的机制基础尚不完全清楚。在 amrZ 缺失突变体和表达 DNA 结合缺陷 AmrZ 的菌株中观察到 pslA 表达升高。AmrZ 是一种转录因子，可正向调节菌毛运动和藻酸盐合成，这两种表型都与铜绿假单胞菌生物膜的发展有关。AmrZ 在体外直接与 pslA 启动子结合，分子分析表明 AmrZ 通过结合重叠启动子的位点来抑制 psl 的表达。非粘液型菌株中 amrZ 的表达改变影响了生物膜的结构和架构，因为在低 AmrZ 产生时观察到结构化的微菌落，而在 AmrZ 过表达时则观察到扁平的生物膜。这些生物膜表型与 Psl 水平相关，因为我们观察到 amrZ 突变体中 Psl 的产生增加，而 amrZ 过表达菌株中 Psl 的产生减少。这些观察结果支持了这样一种假设，即 AmrZ 是一种多功能调节剂，通过抑制 psl 操纵子，同时激活 algD 操纵子，介导铜绿假单胞菌生物膜感染从定植到慢性生物膜的转变。
