2010 journal article
Fur Negatively Regulates hns and Is Required for the Expression of HilA and Virulence in Salmonella enterica Serovar Typhimurium
JOURNAL OF BACTERIOLOGY, 193(2), 497–505.
MeSH headings : Animals; Bacterial Proteins / biosynthesis; Bacterial Proteins / genetics; Bacterial Proteins / metabolism; Chromatin Immunoprecipitation; DNA, Bacterial / metabolism; DNA-Binding Proteins / biosynthesis; DNA-Binding Proteins / metabolism; Disease Models, Animal; Gene Expression Regulation, Bacterial; Gene Knockout Techniques; Genes, Bacterial; Genomic Islands; Mice; Mice, Inbred C3H; Operon; Protein Binding; Repressor Proteins / genetics; Repressor Proteins / metabolism; Salmonella Infections, Animal / microbiology; Salmonella typhimurium / pathogenicity; Salmonella typhimurium / physiology; Survival Analysis; Trans-Activators / biosynthesis; Transcription Factors / biosynthesis; Virulence; Virulence Factors / biosynthesis
TL;DR:
Fur is required for virulence in Salmonella enterica serovar Typhimurium and that Fur is necessary for the activation of hilA, as well as of other HilA-dependent genes, invF and sipC, and chromatin immunoprecipitation was used to show that Fur bound to the upstream region of hns in a metal-dependent fashion.
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UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Source: Web Of Science
Added: August 6, 2018
ABSTRACT Iron is an essential element for the survival of living cells. However, excess iron is toxic, and its uptake is exquisitely regulated by the ferric uptake regulator, Fur. In Salmonella , the Salmonella pathogenicity island 1 (SPI-1) encodes a type three secretion system, which is required for invasion of host epithelial cells in the small intestine. A major activator of SPI-1 is HilA, which is encoded within SPI-1. One known regulator of hilA is Fur. The mechanism of hilA regulation by Fur is unknown. We report here that Fur is required for virulence in Salmonella enterica serovar Typhimurium and that Fur is required for the activation of hilA , as well as of other HilA-dependent genes, invF and sipC . The Fur-dependent regulation of hilA was independent of PhoP, a known repressor of hilA . Instead, the expression of the gene coding for the histone-like protein, hns , was significantly derepressed in the fur mutant. Indeed, the activation of hilA by Fur was dependent on 28 nucleotides located upstream of hns . Moreover, we used chromatin immunoprecipitation to show that Fur bound, in vivo , to the upstream region of hns in a metal-dependent fashion. Finally, deletion of fur in an hns mutant resulted in Fur-independent activation of hilA . In conclusion, Fur activates hilA by repressing the expression of hns .