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鉴定 Vibrio furnissii 利用去铁胺 B 作为外源性铁载体所需的基因 desR 和 desA。

Identification of genes, desR and desA, required for utilization of desferrioxamine B as a xenosiderophore in Vibrio furnissii.

机构信息

College of Pharmaceutical Sciences, Matsuyama University, Bunkyo-cho, Ehime, Japan.

出版信息

Biol Pharm Bull. 2011;34(4):570-4. doi: 10.1248/bpb.34.570.

Abstract

We found that Vibrio (V.) furnissii ATCC35016 can gain iron through a xenosiderophore desferrioxamine B (DFOB) for its growth under iron-limiting conditions, concurrent with the expression of the 79-kDa iron-repressible outer membrane protein (IROMP) in response to the presence of DFOB. Based on the sequence of the ferrioxamine B (an iron-bound form of DFOB) receptor gene in V. vulnificus, two V. furnissii genes, termed desA and desR, encoding the 79-kDa IROMP and AraC-type transcriptional regulator, respectively, were identified and cloned. Nucleotide sequences located in the promoter regions of both desR and desA predicted the presence of consensus ferric uptake regulation (Fur)-binding sequences. The transcription of both genes was negatively regulated by exogenous iron levels. Deletion of the desA gene abolished the ability of V. furnissii to utilize DFOB, and neither desA mRNA nor DesA was detected in the deletion mutant of desR regardless of the presence of DFOB. The functions of DesA and DesR as the ferrioxamine B receptor and transcriptional activator for desA, respectively, were confirmed by complementation of desA and desR deletion mutants.

摘要

我们发现,在缺铁条件下,Vibrio (V.) furnissii ATCC35016 可以通过外源性铁载体去铁胺 B (DFOB) 获得铁,同时响应 DFOB 的存在表达 79kDa 铁抑制性外膜蛋白 (IROMP)。基于 V. vulnificus 中铁结合形式的 DFOB 受体基因的序列,鉴定并克隆了两个 V. furnissii 基因,分别称为 desA 和 desR,分别编码 79kDa 的 IROMP 和 AraC 型转录调节因子。位于 desR 和 desA 启动子区域的核苷酸序列预测存在共识的亚铁摄取调节 (Fur) 结合序列。这两个基因的转录均受外源性铁水平的负调控。缺失 desA 基因会使 V. furnissii 丧失利用 DFOB 的能力,并且无论是否存在 DFOB,在 desR 的缺失突变体中都检测不到 desA mRNA 或 DesA。通过 desA 和 desR 缺失突变体的互补,证实了 DesA 和 DesR 分别作为铁载体去铁胺 B 的受体和 desA 的转录激活因子的功能。

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