The Vibrio cholerae VctPDGC system transports catechol siderophores and a siderophore-free iron ligand.
The Vibrio cholerae VctPDGC system transports catechol siderophores and a siderophore-free iron ligand.
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DOI：
10.1111/j.1365-2958.2011.07775.x
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发表时间：
2011-09
影响因子：
3.6
通讯作者：
Payne SM
中科院分区：
文献类型：
--
作者：
Wyckoff EE;Payne SM
霍乱弧菌是霍乱的病原体，对铁有绝对的需求。它运输儿茶酚铁载体弧菌素，它合成和分泌，和肠杆菌素。这些铁载体通过两种周质结合蛋白依赖性ABC转运蛋白VctPDGC或ViuPDGC之一转运穿过内膜。我们在这里表明，这些内膜运输系统，VctPDGC，也促进铁的收购在铁载体的情况下。携带vctPDGC基因的质粒刺激了不产生铁载体的福氏志贺菌突变体在丰富和基本培养基中的生长。vctPDGC还刺激了E.大肠杆菌肠杆菌素生物合成突变体在低铁培养基中的作用，这种作用不需要feoB，tonB或aroB。在周质结合蛋白VctP的酪氨酸苯丙氨酸取代没有改变肠杆菌素的运输，但消除了生长刺激铁载体的情况下。这些数据表明，VctPDGC系统具有运输儿茶酚铁载体和无铁载体铁配体的能力。我们还表明，VctPDGC是以前未确定的铁载体独立的铁转运V. cholesterol，这似乎完成了V. cholesterol的铁转运系统的列表。
Vibrio cholerae, the causative agent of cholera, has an absolute requirement for iron. It transports the catechol siderophores vibriobactin, which it synthesizes and secretes, and enterobactin. These siderophores are transported across the inner membrane by one of two periplasmic binding protein-dependent ABC transporters, VctPDGC or ViuPDGC. We show here that one of these inner membrane transport systems, VctPDGC, also promotes iron acquisition in the absence of siderophores. Plasmids carrying the vctPDGC genes stimulated growth in both rich and minimal media of a Shigella flexneri mutant that produces no siderophores. vctPDGC also stimulated the growth of an E. coli enterobactin biosynthetic mutant in low iron medium, and this effect did not require feoB, tonB or aroB. A tyrosine to phenylalanine substitution in the periplasmic binding protein VctP did not alter enterobactin transport, but eliminated growth stimulation in the absence of a siderophore. These data suggest that the VctPDGC system has the capacity to transport both catechol siderophores and a siderophore-free iron ligand. We also show that VctPDGC is the previously unidentified siderophore-independent iron transporter in V. cholerae, and this appears to complete the list of iron transport systems in V. cholerae.
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影响因子：
3.6
作者：
Makui, H;Roig, E;Cellier, MFM
通讯作者：
Cellier, MFM
影响因子：
3.2
作者：
Kehres, DG;Janakiraman, A;Maguire, ME
通讯作者：
Maguire, ME
影响因子：
3.2
作者：
Mey, Alexandra R.;Wyckoff, Elizabeth E.;Payne, Shelley M.
通讯作者：
Payne, Shelley M.
大肠杆菌K-12的构造框架，单基因敲除突变体：Keio Collection。
影响因子：
9.9
作者：
通讯作者：
--
影响因子：
3.2
作者：
CHANG, ACY;COHEN, SN
通讯作者：
COHEN, SN