Weak Organic Acids Decrease Borrelia burgdorferi Cytoplasmic pH, Eliciting an Acid Stress Response and Impacting RpoN- and RpoS-Dependent Gene Expression.
Weak Organic Acids Decrease Borrelia burgdorferi Cytoplasmic pH, Eliciting an Acid Stress Response and Impacting RpoN- and RpoS-Dependent Gene Expression.
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DOI：
10.3389/fmicb.2017.01734
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发表时间：
2017
影响因子：
5.2
通讯作者：
Gherardini FC
中科院分区：
文献类型：
--
作者：
Dulebohn DP;Richards CL;Su H;Lawrence KA;Gherardini FC
螺旋体伯氏疏螺旋体存活于其蜱虫载体肩突硬蜱中或各种宿主中。为了在这些不同的生态位之间过渡并生存，B。burgdorferi改变其基因表达以响应环境的生化和生理线索。B的暴露。burgdorferi对弱一元羧酸有机酸，包括在进食蜱的血粉中检测到的那些，降低了B的细胞质pH。Burgdorferi体外培养。细胞质pH值的降低诱导了编码酶的基因的表达，这些酶已被证明可以恢复其他细菌中的pH稳态。这些包括假定的耦合质子/阳离子交换剂，一个假定的Na+/H+反向转运蛋白，一个中和缓冲转运蛋白，氨基酸脱氨酶和质子输出液泡型VoV 1 ATP酶。本报告中提供的数据表明，酸应激反应触发了RpoN和RpoS依赖性基因的表达，包括重要的毒力因子，如外表面蛋白C（OspC），BBA 66和一些BosR（疏螺旋体氧化应激调节因子）依赖性基因。由于毒力因子的表达，如OspC，通过RpoS与一般细胞应激反应和细胞生理学紧密相连，因此很难在明显是多因素和复杂的调控网络中分离促进传播的条件。
The spirochete Borrelia burgdorferi survives in its tick vector, Ixodes scapularis, or within various hosts. To transition between and survive in these distinct niches, B. burgdorferi changes its gene expression in response to environmental cues, both biochemical and physiological. Exposure of B. burgdorferi to weak monocarboxylic organic acids, including those detected in the blood meal of fed ticks, decreased the cytoplasmic pH of B. burgdorferi in vitro. A decrease in the cytoplasmic pH induced the expression of genes encoding enzymes that have been shown to restore pH homeostasis in other bacteria. These include putative coupled proton/cation exchangers, a putative Na+/H+ antiporter, a neutralizing buffer transporter, an amino acid deaminase and a proton exporting vacuolar-type VoV1 ATPase. Data presented in this report suggested that the acid stress response triggered the expression of RpoN- and RpoS-dependent genes including important virulence factors such as outer surface protein C (OspC), BBA66, and some BosR (Borrelia oxidative stress regulator)-dependent genes. Because the expression of virulence factors, like OspC, are so tightly connected by RpoS to general cellular stress responses and cell physiology, it is difficult to separate transmission-promoting conditions in what is clearly a multifactorial and complex regulatory web.