• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>MicrobiologyOpen >Two parallel pathways for ferric and ferrous iron acquisition support growth and virulence of the intracellular pathogen Francisella tularensis Schu S4
【24h】

Two parallel pathways for ferric and ferrous iron acquisition support growth and virulence of the intracellular pathogen Francisella tularensis Schu S4

机译：铁和二价铁获取的两个平行途径支持细胞内病原菌弗朗西斯菌Tchuensis Schu S4的生长和毒力

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Abstract Iron acquisition mechanisms in Francisella tularensis , the causative agent of tularemia, include the Francisella siderophore locus ( fsl) siderophore operon and a ferrous iron?￠????transport system comprising outer-membrane protein FupA and inner-membrane transporter FeoB. To characterize these mechanisms and to identify any additional iron uptake systems in the virulent subspecies tularensis , single and double deletions were generated in the fsl and feo iron acquisition systems of the strain Schu S4. Deletion of the entire fsl operon caused loss of siderophore production that could be restored by complementation with the biosynthetic genes fslA and fslC and Major Facilitator Superfamily (MFS) transporter gene fslB . 55 Fe-transport assays demonstrated that siderophore-iron uptake required the receptor FslE and MFS transporter FslD. A ???? feoB ?￠???2 mutation resulted in loss of ability to transport ferrous iron ( 55 Fe 2+ ). A ???? feoB ?￠???2 ???? fslA mutant that required added exogenous siderophore for growth in vitro was unable to grow within tissue culture cells and was avirulent in mice, indicating that no compensatory cryptic iron uptake systems were induced in vivo. These studies demonstrate that the fsl and feo pathways function independently and operate in parallel to effectively support virulence of F. tularensis .
机译：摘要图拉弗朗斯病的病原体图拉弗朗西斯菌的铁捕获机制包括弗朗西斯菌铁载体（fsl）铁载体和含铁的铁转运体系，该转运体系由外膜蛋白FupA和内膜转运蛋白FeoB组成。为了表征这些机制并鉴定强毒亚种tularensis中的任何其他铁吸收系统，在Schu S4菌株的fsl和feo铁采集系统中产生了单缺失和双缺失。整个fsl操纵子的缺失引起铁载体产量的损失，可以通过与生物合成基因fslA和fslC以及主要促进者超家族（MFS）转运蛋白基因fslB互补来恢复。 55 Fe转运分析表明，铁矿铁的吸收需要受体FslE和MFS转运蛋白FslD。一种 ？？？？ feoBα2突变导致输运亚铁离子（55 Fe 2+）的能力丧失。一种 ？？？？ feoB？￠ ??? 2 ????要求添加外源铁载体体外生长的fslA突变体无法在组织培养细胞内生长，并且在小鼠中无毒，表明体内没有诱导代偿性隐性铁摄取系统。这些研究表明，fsl和feo途径独立发挥作用，并并行运行，以有效地支持土桑的毒性。

著录项

相似文献

  • 外文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号