The role of fur in the acid tolerance response of Salmonella typhimurium is physiologically and genetically separable from its role in iron acquisition

The role of fur in the acid tolerance response of Salmonella typhimurium is physiologically and genetically separable from its role in iron acquisition
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DOI:
10.1128/jb.178.19.5683-5691.1996
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发表时间:
1996-10-01
影响因子:
3.2
通讯作者:
Foster, JW
Foster, JW
中科院分区:
生物学3区
文献类型:
--
作者:
Hall, HK;Foster, JW

文献摘要

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鼠伤寒沙门氏菌对低pH值的反应包括一个称为耐酸性反应(ATR)的低pH值保护系统。铁调节蛋白Fur与ATR有关,因为Fur突变体是酸敏感的,并引起几种酸休克蛋白的表达改变(J.W. Foster,J. Bacteriol. 173:6896-6902,1991)。我们已经确定,毛皮突变的酸敏感表型确实是由于毛皮中的缺陷,可以通过含有毛皮(+)的质粒进行补充。然而,细胞铁状态的变化本身并不触发ATR。细胞显然需要暴露于低pH以诱导耐酸性。发现Fur在酸耐受性中的作用超出了调节铁的获得。在毛皮中的突变将组氨酸90转化为精氨酸(H90 R)消除了毛皮介导的铁对肠螯合素产生的调节,并解除了iroA-lacZ融合的调节,但对酸耐受性没有影响。H90 R铁盲Fur蛋白还介导了几种Fur依赖性酸休克蛋白的酸休克诱导和hyd位点的酸控制。此外,组成性抑制铁调节基因的毛皮超阻遏物介导正常的毛皮依赖的耐酸性和pH值控制的基因表达。结果表明,酸敏感和铁敏感机制的毛皮是可分离的突变和加强的概念,毛皮作为一个主要的全球调节细胞。
The response of Salmonella typhimurium to low pH includes a low-pH protection system called the acid tolerance response (ATR). The iron-regulatory protein Fur has been implicated in the ATR since fur mutants are acid sensitive and cause altered expression of several acid shock proteins (J. W. Foster, J. Bacteriol. 173:6896-6902, 1991). We have determined that the acid-sensitive phenotype of fur mutations is indeed due to a defect in Fur that can be complemented by a fur(+)-containing plasmid. However, changes in cellular iron status alone did not trigger the ATR. Cells clearly required exposure to low pH in order to induce acid tolerance. The role of Fur in acid tolerance was found to extend beyond regulating iron acquisition. A mutation in fur converting histidine 90 to an arginine (H90R) eliminated Fur-mediated iron regulation of enterochelin production and deregulated an iroA-lacZ fusion but had no effect on acid tolerance. The H90R iron-blind Fur protein also mediated acid shock induction of several Fur-dependent acid shock proteins and acid control of the hyd locus. In addition, a Fur superrepressor that constitutively repressed iron-regulated genes mediated normal Fur-dependent acid tolerance and pH-controlled gene expression. The results indicate the acid-sensing and iron-sensing mechanisms of Fur are separable by mutation and reinforce the concept of Fur as a major global regulator in the cell.