YdiV regulates Escherichia coli ferric uptake by manipulating the DNA-binding ability of Fur in a SlyD-dependent manner.

YdiV regulates Escherichia coli ferric uptake by manipulating the DNA-binding ability of Fur in a SlyD-dependent manner.
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DOI:
10.1093/nar/gkaa696
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发表时间:
2020-09-25
影响因子:
14.9
通讯作者:
Gu L
Gu L
中科院分区:
生物学2区
文献类型:
--
作者:
Zhang F;Li B;Dong H;Chen M;Yao S;Li J;Zhang H;Liu X;Wang H;Song N;Zhang K;Du N;Xu S;Gu L

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铁对所有细菌都是必需的。在大多数细菌中,细胞内铁稳态由铁摄取调节剂Fur严格调节。然而,如何毛皮激活铁吸收系统在缺铁没有完全阐明。在这项研究中,我们发现,YdiV,鞭毛基因抑制剂,参与铁稳态在大肠杆菌。缺铁引发YdiV的过度表达。然后高水平的YdiV将Fur转化为不以肽基-脯氨酰顺反异构酶SlyD依赖性方式结合DNA的新形式。因此,YdiV,SlyD和Fur的合作激活铁摄取系统的基因表达在缺铁的条件下。细菌侵袭实验也证明ydiV和slyD对尿路致病性大肠杆菌的存活和生长都是必需的。膀胱上皮细胞中的大肠杆菌。这揭示了一种机制,其中YdiV不仅抑制鞭毛表达,使E.大肠杆菌对宿主免疫系统是不可见的,但它也促进铁的获得,以帮助大肠杆菌。大肠杆菌克服宿主营养免疫。
Iron is essential for all bacteria. In most bacteria, intracellular iron homeostasis is tightly regulated by the ferric uptake regulator Fur. However, how Fur activates the iron-uptake system during iron deficiency is not fully elucidated. In this study, we found that YdiV, the flagella gene inhibitor, is involved in iron homeostasis in Escherichia coli. Iron deficiency triggers overexpression of YdiV. High levels of YdiV then transforms Fur into a novel form which does not bind DNA in a peptidyl-prolyl cis-trans isomerase SlyD dependent manner. Thus, the cooperation of YdiV, SlyD and Fur activates the gene expression of iron-uptake systems under conditions of iron deficiency. Bacterial invasion assays also demonstrated that both ydiV and slyD are necessary for the survival and growth of uropathogenic E. coli in bladder epithelial cells. This reveals a mechanism where YdiV not only represses flagella expression to make E. coli invisible to the host immune system, but it also promotes iron acquisition to help E. coli overcome host nutritional immunity.
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