Dataset Information

The FeoC protein leads to high cellular levels of the Fe(II) transporter FeoB by preventing FtsH protease regulation of FeoB in Salmonella enterica.

ABSTRACT: In the gammaproteobacteria, the FeoA, FeoB, and FeoC proteins constitute the Feo system, which mediates ferrous iron [Fe(II)] import. Of these Feo proteins, FeoB is an inner membrane Fe(II) transporter that is aided by the small protein FeoA. However, the role of another small protein, FeoC, has remained unknown. Here we report that the FeoC protein is necessary for FeoB protein-mediated Fe(II) uptake in Salmonella experiencing low levels of oxygen and iron. The FeoC protein was found to directly bind to the FeoB transporter, leading to high cellular levels of FeoB. Depletion of the FtsH protease enabled high levels of FeoB in the absence of FeoC, suggesting that the FeoC protein protects the FeoB transporter from FtsH-mediated proteolysis. Our present study provides a singular example of bacteria that can control expression of iron uptake systems posttranslationally by employing a small iron transporter-binding protein.

SUBMITTER: Kim H

PROVIDER: S-EPMC3719545 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature

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The FeoC protein leads to high cellular levels of the Fe(II) transporter FeoB by preventing FtsH protease regulation of FeoB in Salmonella enterica.

Kim Hyunkeun H Lee Hwiseop H Shin Dongwoo D

Journal of bacteriology 20130524 15

In the gammaproteobacteria, the FeoA, FeoB, and FeoC proteins constitute the Feo system, which mediates ferrous iron [Fe(II)] import. Of these Feo proteins, FeoB is an inner membrane Fe(II) transporter that is aided by the small protein FeoA. However, the role of another small protein, FeoC, has remained unknown. Here we report that the FeoC protein is necessary for FeoB protein-mediated Fe(II) uptake in Salmonella experiencing low levels of oxygen and iron. The FeoC protein was found to directl ...[more]

PMID: 23708131

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Project description:BACKGROUND:Intestinal fibrosis is a common and serious complication of Crohn's disease characterized by the accumulation of fibroblasts, deposition of extracellular matrix, and formation of scar tissue. Although many factors including cytokines and proteases contribute to the development of intestinal fibrosis, the initiating mechanisms and the complex interplay between these factors remain unclear. METHODS:Chronic infection of mice with Salmonella enterica serovar Typhimurium was used to induce intestinal fibrosis. A murine protease-specific CLIP-CHIP microarray analysis was employed to assess regulation of proteases and protease inhibitors. To confirm up- or downregulation during fibrosis, we performed quantitative real-time polymerase chain reaction (PCR) and immunohistochemical stainings in mouse tissue and tissue from patients with inflammatory bowel disease. In vitro infections were used to demonstrate a direct effect of bacterial infection in the regulation of proteases. RESULTS:Mice develop severe and persistent intestinal fibrosis upon chronic infection with Salmonella enterica serovar Typhimurium, mimicking the pathology of human disease. Microarray analyses revealed 56 up- and 40 downregulated proteases and protease inhibitors in fibrotic cecal tissue. Various matrix metalloproteases, serine proteases, cysteine proteases, and protease inhibitors were regulated in the fibrotic tissue, 22 of which were confirmed by quantitative real-time PCR. Proteases demonstrated site-specific staining patterns in intestinal fibrotic tissue from mice and in tissue from human inflammatory bowel disease patients. Finally, we show in vitro that Salmonella infection directly induces protease expression in macrophages and epithelial cells but not in fibroblasts. CONCLUSIONS:In summary, we show that chronic Salmonella infection regulates proteases and protease inhibitors during tissue fibrosis in vivo and in vitro, and therefore this model is well suited to investigating the role of proteases in intestinal fibrosis.

Dataset Information

The FeoC protein leads to high cellular levels of the Fe(II) transporter FeoB by preventing FtsH protease regulation of FeoB in Salmonella enterica.

Publications

The FeoC protein leads to high cellular levels of the Fe(II) transporter FeoB by preventing FtsH protease regulation of FeoB in Salmonella enterica.

Similar Datasets

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