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首页> 外文期刊>Infection and immunity >Expression of BfrH, a Putative Siderophore Receptor of Bordetella bronchiseptica, Is Regulated by Iron, Fur1, and the Extracellular Function Sigma Factor EcfI
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Expression of BfrH, a Putative Siderophore Receptor of Bordetella bronchiseptica, Is Regulated by Iron, Fur1, and the Extracellular Function Sigma Factor EcfI

机译：铁，Fur1和细胞外功能西格玛因子EcfI调节支气管败血性博德特氏菌的假定铁载体受体BfrH的表达。

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Iron (Fe) in soluble elemental form is found in the tissues and fluids of animals at concentrations insufficient for sustaining growth of bacteria. Consequently, to promote colonization and persistence, pathogenic bacteria evolved a myriad of scavenging mechanisms to acquire Fe from the host. Bordetella bronchiseptica, the etiologic agent of upper respiratory infections in a wide range of mammalian hosts, expresses a number of proteins for acquisition of Fe. Using proteomic and genomic approaches, three Fe-regulated genes were identified in the bordetellae: bfrH, a gene encoding a putative siderophore receptor; ecfI, a gene encoding a putative extracellular function (ECF) sigma factor; and ecfR, a gene encoding a putative EcfI modulator. All three genes are highly conserved in B. pertussis, B. parapertussis, and B. avium. Genetic analysis revealed that transcription of bfrH was coregulated by ecfI, ecfR, and fur1, one of two fur homologues carried by B. bronchiseptica. Overexpression of ecfI decoupled bfrH from Fe-dependent regulation. In contrast, expression of bfrH was significantly reduced in an ecfI deletion mutant. Deletion of ecfR, however, was correlated with a significant increase in expression of bfrH, due in part to a cis-acting nucleotide sequence within ecfR which likely reduces the frequency of readthrough transcription of bfrH from the Fe-dependent ecfIR promoter. Using a murine competition infection model, bfrH was shown to be required for optimal virulence of B. bronchiseptica. These experiments revealed ecfIR-bfrH as a locus encoding a new member of the growing family of Fe and ECF sigma factor-modulated regulons in the bordetellae.
机译：在动物的组织和体液中发现可溶性元素形式的铁（Fe），其浓度不足以维持细菌的生长。因此，为了促进定植和持久性，病原菌进化出无数种清除机制以从宿主中获取铁。支气管博德特氏菌是多种哺乳动物宿主中上呼吸道感染的病原体，它表达许多蛋白质以获取铁。使用蛋白质组学和基因组学方法，在果蝇中鉴定出三个Fe调控的基因：bfrH，一个编码推定铁载体的基因; ecfI，一种编码假定的细胞外功能（ECF）西格玛​​因子的基因; ecfR，编码推定的EcfI调节剂的基因。这三个基因在百日咳博德特氏菌，副百日咳博德特氏菌和鸟博德特氏菌中都是高度保守的。遗传分析显示bfrH的转录受支气管败血性博德特氏菌携带的两个毛皮同源物中的一个的ecfI，ecfR和fur1调控。 ecfI的过表达使bfrH与铁依赖性调节脱钩。相反，在ecfI缺失突变体中bfrH的表达显着降低。然而，ecfR的缺失与bfrH表达的显着增加相关，部分原因是ecfR内的顺式作用核苷酸序列，其可能降低了Fe依赖性ecfIR启动子对bfrH的通读转录的频率。使用鼠竞争性感染模型，证明bfrH是支气管败血性博德特氏菌最佳毒力所必需的。这些实验揭示了ecfIR-bfrH是编码波尔德族中铁和ECFσ因子调节的调节子的增长家族的新成员的基因座。

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