Fernández Paulina A, Velásquez Felipe, Garcias-Papayani Héctor, Amaya Fernando A, Ortega Jaime, Gómez Sebastián, Santiviago Carlos A, Álvarez Sergio A
Laboratorio de Microbiología, Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile.
Front Microbiol. 2018 Jun 8;9:1220. doi: 10.3389/fmicb.2018.01220. eCollection 2018.
Lipid A is the bioactive component of lipopolysaccharide, and presents a dynamic structure that undergoes modifications in response to environmental signals. Many of these structural modifications influence virulence. This is the case of lipid A hydroxylation, a modification catalyzed by the dioxygenase LpxO. Although it has been established that oxygen is required for lipid A hydroxylation acting as substrate of LpxO in , an additional regulatory role for oxygen in expression has not been described. The existence of this regulation could be relevant considering that faces low oxygen tension during infection. This condition leads to an adaptive response by changing the expression of numerous genes, and transcription factors Fnr and ArcA are major regulators of this process. In this work, we describe for the first time that lipid A hydroxylation and expression are modulated by oxygen availability in serovar Enteritidis (. Enteritidis). Biochemical and genetic analyses indicate that this process is regulated by Fnr and ArcA controlling the expression of . In addition, according to our results, this regulation occurs by direct binding of both transcription factors to specific elements present in the promoter region. Altogether, our observations revealed a novel role for oxygen acting as an environment signal controlling lipid A hydroxylation in . Enteritidis.
脂多糖A是脂多糖的生物活性成分，呈现出一种动态结构，可根据环境信号进行修饰。其中许多结构修饰会影响毒力。脂多糖A羟基化就是这种情况，这是一种由双加氧酶LpxO催化的修饰。尽管已经确定在脂多糖A羟基化作为LpxO的底物时需要氧气，但尚未描述氧气在其表达中的额外调节作用。考虑到在感染过程中面临低氧张力，这种调节的存在可能具有相关性。这种情况会通过改变众多基因的表达引发适应性反应，转录因子Fnr和ArcA是这一过程的主要调节因子。在这项工作中，我们首次描述了肠炎沙门氏菌（肠炎亚种）中脂多糖A羟基化和其表达受氧可用性的调节。生化和遗传分析表明，这一过程由Fnr和ArcA调控，它们控制着其表达。此外，根据我们的结果，这种调节是通过这两种转录因子直接结合到启动子区域中存在的特定元件而发生的。总之，我们的观察结果揭示了氧气作为一种环境信号在肠炎亚种中控制脂多糖A羟基化的新作用。
