Briggs Heather L, Pul Nicolein, Seshadri Rekha, Wilson Mary J, Tersteeg Claudia, Russell-Lodrigue Kasi E, Andoh Masako, Bäumler Andreas J, Samuel James E
Department of Microbial and Molecular Pathogenesis, Texas A&M University System Health Science Center, College Station, TX 77843-1114, USA.
Infect Immun. 2008 May;76(5):2189-201. doi: 10.1128/IAI.01609-07. Epub 2008 Mar 3.
In gram-negative bacteria, iron acquisition proteins are commonly regulated by Fur (ferric uptake regulator), which binds iron-regulated promoters (the Fur box). We hypothesized that Coxiella burnetii requires iron and employs an iron-regulatory system and used various approaches to define a Fur regulon. Cloned C. burnetii fur complemented an Escherichia coli fur deletion mutant. A ferrous iron transporter gene (CBU1766), a putative iron binding protein-encoding gene (CBU0970), and a cation efflux pump gene (CBU1362) were identified by genome annotation and using a Fur titration assay. Bioinformatically predicted Fur box-containing promoters were tested for transcriptional control by iron. Five genes demonstrated at least a twofold induction with minimal iron. Putatively regulated genes were evaluated in a two-plasmid regulator/promoter heterologous expression system. These data suggested a very limited Fur-regulated system in C. burnetii. In an in vitro tissue culture model, a significant increase in bacterial growth was observed with infected cells treated with deferoxamine in comparison to growth under iron-replete conditions. In an iron-overloaded animal model in vivo, the level of bacterial growth detected in the iron-injected animals was significantly decreased in comparison to growth in control animals. In a low-iron-diet animal model, a significant increase in splenomegaly was observed, but no significant change in bacterial growth was identified. The small number of predicted iron acquisition systems, few Fur-regulated genes, and enhanced replication under a decreased iron level predict a requirement of a low level of iron for survival, perhaps to avoid creation of additional reactive oxygen radicals.
在革兰氏阴性菌中,铁摄取蛋白通常受Fur(铁摄取调节蛋白)调控,Fur可结合铁调节启动子(Fur盒)。我们推测伯氏考克斯体需要铁并采用一种铁调节系统,于是运用多种方法来定义Fur调控子。克隆的伯氏考克斯体fur基因可互补大肠杆菌fur缺失突变体。通过基因组注释及Fur滴定试验鉴定出一个亚铁转运蛋白基因(CBU1766)、一个推测的铁结合蛋白编码基因(CBU0970)和一个阳离子外流泵基因(CBU1362)。对通过生物信息学预测的含Fur盒启动子进行了铁介导的转录调控测试。有5个基因在低铁条件下表现出至少两倍的诱导。在一个双质粒调节子/启动子异源表达系统中对推测的受调控基因进行了评估。这些数据表明伯氏考克斯体中Fur调节系统非常有限。在体外组织培养模型中,与铁充足条件下的生长相比,用去铁胺处理的感染细胞中细菌生长显著增加。在体内铁过载动物模型中,与对照动物相比,注射铁的动物体内检测到的细菌生长水平显著降低。在低铁饮食动物模型中,观察到脾脏肿大显著增加,但未发现细菌生长有显著变化。预测的铁摄取系统数量少、Fur调控基因少以及在铁水平降低时复制增强,预示着生存需要低水平的铁,这可能是为了避免产生额外的活性氧自由基。