Reference : Hierarchical regulation of the NikR-mediated nickel response in Helicobacter pylori.
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/10993/26357
Hierarchical regulation of the NikR-mediated nickel response in Helicobacter pylori.
English
Muller, Cecile [Institut Pasteur (paris) > Dept Microbiol, Unite Pathogenese Helicobacter]
Bahlawane, Christelle mailto [Commissariat à l'Energie Atomique (Saclay) - CEA > UMR 5249, Lab Chim & Biol Met]
Aubert, Sylvie [Institut Pasteur (Paris) > Dept Microbiol, Unite Pathogenese Helicobacter]
Delay, Catherine Marie [Institut pasteur (Paris) > Dept Microbiol, Unite Pathogenese Helicobacter]
Schauer, Kristine [Institut pasteur (paris) > Dept Microbiol, Unite Pathogenese Helicobacter]
Michaud-Soret, Isabelle [Commissariat à l'Energie Atomique (Saclay) - CEA > UMR 5249, Lab Chim & Biol Met]
De Reuse, Hilde [Institut Pasteur (Paris) > Dept Microbiol, Unite Pathogenese Helicobacter,]
2011
Nucleic acids research
39
17
7564-75
Yes (verified by ORBilu)
International
0305-1048
1362-4962
England
[en] Bacterial Proteins/metabolism ; Gene Expression Regulation, Bacterial/drug effects ; Helicobacter pylori/drug effects/genetics/metabolism ; Kinetics ; Nickel/pharmacology ; Repressor Proteins/metabolism ; Transcription, Genetic/drug effects
[en] Nickel is an essential metal for Helicobacter pylori, as it is the co-factor of two enzymes crucial for colonization, urease and hydrogenase. Nickel is taken up by specific transporters and its intracellular homeostasis depends on nickel-binding proteins to avoid toxicity. Nickel trafficking is controlled by the Ni(II)-dependent transcriptional regulator NikR. In contrast to other NikR proteins, NikR from H. pylori is a pleiotropic regulator that depending on the target gene acts as an activator or a repressor. We systematically quantified the in vivo Ni(2+)-NikR response of 11 direct NikR targets that encode functions related to nickel metabolism, four activated and seven repressed genes. Among these, four targets were characterized for the first time (hpn, hpn-like, hydA and hspA) and NikR binding to their promoter regions was demonstrated by electrophoretic mobility shift assays. We found that NikR-dependent repression was generally set up at higher nickel concentrations than activation. Kinetics of the regulation revealed a gradual and temporal NikR-mediated response to nickel where activation of nickel-protection mechanisms takes place before repression of nickel uptake. Our in vivo study demonstrates, for the first time, a chronological hierarchy in the NikR-dependent transcriptional response to nickel that is coherent with the control of nickel homeostasis in H. pylori.
http://hdl.handle.net/10993/26357

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