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首页> 外文期刊>Journal of bacteriology >The BfeR Regulator Mediates Enterobactin-Inducible Expression of Bordetella Enterobactin Utilization Genes
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The BfeR Regulator Mediates Enterobactin-Inducible Expression of Bordetella Enterobactin Utilization Genes

机译：BfeR调节剂介导鲍氏杆菌肠杆菌素利用基因的肠杆菌素诱导表达。

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Utilization of the enterobactin siderophore by the respiratory pathogens Bordetella pertussis and Bordetella bronchiseptica is dependent on the BfeA outer membrane receptor. This study determined that production of BfeA was increased significantly in iron-starved bacteria upon supplementation of cultures with enterobactin. A 1.01-kb open reading frame, designated bfeR, encoding a predicted positive transcriptional regulator of the AraC family was identified upstream and divergently oriented from bfeA. In iron-depleted cultures containing enterobactin, a Bordetella bfeR mutant exhibited markedly decreased BfeA receptor production compared to that of the wild-type strain. Additionally, B. pertussis and B. bronchiseptica bfeR mutants exhibited impaired growth with ferric enterobactin as the sole source of iron, demonstrating that effective enterobactin utilization is bfeR dependent. Transcriptional analysis using bfeA-lacZ reporter fusions in wild-type strains demonstrated that bfeA transcription was stimulated in iron-depleted conditions in the presence of enterobactin, compared to modest expression levels in cultures lacking enterobactin. In contrast, bfeA transcription in B. pertussis and B. bronchiseptica bfeR mutants was completely unresponsive to the enterobactin inducer. bfeA transcriptional analyses of a bfeA mutant demonstrated that induction by enterobactin did not require BfeA receptor-mediated uptake of the siderophore. These studies establish that bfeR encodes an enterobactin-dependent positive regulator of bfeA transcription in these Bordetella species.
机译：呼吸道病原菌百日咳博德特氏菌和支气管败血博德特氏菌对肠细菌素铁载体的利用取决于BfeA外膜受体。这项研究确定，补充肠杆菌素后，铁饥饿的细菌中BfeA的产量显着增加。在上游发现了一个1.01kb的开放阅读框，命名为 bfeR ，它编码AraC家族的预期正转录调节子，并从 bfeA 定向。与野生型菌株相比，在含有肠杆菌素的贫铁培养物中，博德特氏菌bfeR 突变体的BfeA受体产生明显减少。此外， B。百日咳和 B。支气管败血性bfeR 突变体以铁肠铁蛋白作为唯一铁源显示出生长受阻，表明有效的肠铁蛋白利用是 bfeR 依赖的。在野生型菌株中使用 bfeA - lacZ 报告基因融合体进行转录分析，结果表明，在存在铁链菌素的条件下，铁缺乏条件下刺激了 bfeA 转录与缺乏肠杆菌素的培养物中适度的表达水平相比。相反， B中的 bfeA 转录。百日咳和 B。支气管败血病bfeR 突变体对肠杆菌素诱导剂完全无反应。 bfeA 突变体的 bfeA 转录分析表明，肠抑菌素的诱导不需要BfeA受体介导的铁载体的摄取。这些研究表明， bfeR 在这些 Bordetella 物种中编码一种依赖于肠细菌素的 bfeA 转录正调控子。

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