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A Single Nucleotide Change Affects Fur-Dependent Regulation of sodB in H. pylori

By Beth M. Carpenter, Hanan Gancz, Reyda P. Gonzalez-Nieves, Abby L. West, Jeannette M. Whitmire, Sarah L. J. Michel and D. Scott Merrell


Helicobacter pylori is a significant human pathogen that has adapted to survive the many stresses found within the gastric environment. Superoxide Dismutase (SodB) is an important factor that helps H. pylori combat oxidative stress. sodB was previously shown to be repressed by the Ferric Uptake Regulator (Fur) in the absence of iron (apo-Fur regulation) [1]. Herein, we show that apo regulation is not fully conserved among all strains of H. pylori. apo-Fur dependent changes in sodB expression are not observed under iron deplete conditions in H. pylori strains G27, HPAG1, or J99. However, Fur regulation of pfr and amiE occurs as expected. Comparative analysis of the Fur coding sequence between G27 and 26695 revealed a single amino acid difference, which was not responsible for the altered sodB regulation. Comparison of the sodB promoters from G27 and 26695 also revealed a single nucleotide difference within the predicted Fur binding site. Alteration of this nucleotide in G27 to that of 26695 restored apo-Fur dependent sodB regulation, indicating that a single base difference is at least partially responsible for the difference in sodB regulation observed among these H. pylori strains. Fur binding studies revealed that alteration of this single nucleotide in G27 increased the affinity of Fur for the sodB promoter. Additionally, the single base change in G27 enabled the sodB promoter to bind to apo-Fur with affinities similar to the 26695 sodB promoter. Taken together these data indicate that this nucleotide residue is important for direct apo-Fur binding to the sodB promoter

Topics: Research Article
Publisher: Public Library of Science
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Provided by: PubMed Central

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  1. (2005). Activation of beta-catenin by carcinogenic Helicobacter pylori.
  2. (2003). An anti-repression Fur operator upstream of the promoter is required for iron-mediated transcriptional autoregulation in Helicobacter pylori.
  3. (2002). Autoregulation of Helicobacter pylori Fur revealed by functional analysis of the iron-binding site.
  4. (1998). Binding of the Fur (ferric uptake regulator) repressor of Escherichia coli to arrays of the GATAAT sequence.
  5. (1989). Campylobacter pylori virulence factors in gnotobiotic piglets.
  6. (2003). Characterization of Helicobacter pylori nickel metabolism accessory proteins needed for maturation of both urease and hydrogenase.
  7. (1998). Cloning and characterization of the fur gene from Helicobacter pylori.
  8. (2006). der Ende A
  9. (2003). Differential regulation of amidase- and formamidase-mediated ammonia production by the Helicobacter pylori fur repressor.
  10. (2007). Expanding the Helicobacter pylori genetic toolbox: modification of an endogenous plasmid for use as a transcriptional reporter and complementation vector.
  11. (2006). Expression of the Escherichia coli IrgA homolog adhesin is regulated by the ferric uptake regulation protein.
  12. (1996). FACS-optimized mutants of the green fluorescent protein (GFP).
  13. (2003). Gene expression profiling of Helicobacter pylori reveals a growth-phase-dependent switch in virulence gene expression.
  14. (1999). Genomicsequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori.
  15. (1990). Helicobacter pylori and the pathogenesis of gastroduodenal inflammation.
  16. (1997). Helicobacter pylori.
  17. (2005). In vitro analysis of protein-operator interactions of the NikR and Fur metal-responsive regulators of coregulated genes in Helicobacter pylori.
  18. (1997). Introduction of unmarked mutations in the Helicobacter pylori vacA gene with a sucrose sensitivity marker.
  19. (2006). Iron and pH homeostasis intersect at the level of Fur regulation in the gastric pathogen Helicobacter pylori.
  20. (2001). Iron-dependent transcription of the frpB gene of Helicobacter pylori is controlled by the Fur repressor protein.
  21. (2005). Ironresponsive regulation of the Helicobacter pylori iron-cofactored superoxide dismutase SodB is mediated by Fur.
  22. (1993). Molecular characterization of the 128-kDa immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer.
  23. (1988). Multiple sequence alignment with hierarchical clustering. Nucleic Acids Res 16: 10881–10890. sodB in H.
  24. (2000). One-step inactivation of chromosomal genes in Escherichia coli K-12 using PCR products.
  25. (1987). Operator sequences of the aerobactin operon of plasmid ColV-K30 binding the ferric uptake regulation (fur) repressor.
  26. (2005). Oxidative stress defense mechanisms to counter iron-promoted DNA damage in Helicobacter pylori.
  27. (1993). Purification of Helicobacter pylori superoxide dismutase and cloning and sequencing of the gene.
  28. (2004). Quantitation of H. pylori cytotoxin mRNA by real-time RT-PCR shows a wide expression range that does not correlate with promoter sequences.
  29. (2004). Responsiveness to acidity via metal ion regulators mediates virulence in the gastric pathogen Helicobacter pylori.
  30. (2008). Sodium chloride affects Helicobacter pylori growth and gene expression.
  31. (2005). Strain-specific expression profiles of virulence genes in Helicobacter pylori during infection of gastric epithelial cells and granulocytes.
  32. (1990). Superoxide dismutase and Fenton chemistry. Reaction of ferric-EDTA complex and ferric-bipyridyl complex with hydrogen peroxide without the apparent formation of iron(II).
  33. (2001). Superoxide dismutase-deficient mutants of Helicobacter pylori are hypersensitive to oxidative stress and defective in host colonization.
  34. (2006). The complete genome sequence of a chronic atrophic gastritis Helicobacter pylori strain: evolution during disease progression.
  35. (1997). The complete genome sequence of the gastric pathogen Helicobacter pylori.
  36. (2007). The CrdRS (HP1365-HP1364) twocomponent system is not involved in pH-responsive gene regulation in the Helicobacter pylori Strains 26695 and G27.
  37. (2001). The Fur repressor controls transcription of iron-activated and -repressed genes in Helicobacter pylori.M o l

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