Literature DB >> 22698670

Helicobacter pylori hydrogenase accessory protein HypA and urease accessory protein UreG compete with each other for UreE recognition.

Stéphane L Benoit1, Jonathan L McMurry, Stephanie A Hill, Robert J Maier.   

Abstract

BACKGROUND: The gastric pathogen Helicobacter pylori relies on nickel-containing urease and hydrogenase enzymes in order to colonize the host. Incorporation of Ni(2+) into urease is essential for the function of the enzyme and requires the action of several accessory proteins, including the hydrogenase accessory proteins HypA and HypB and the urease accessory proteins UreE, UreF, UreG and UreH.
METHODS: Optical biosensing methods (biolayer interferometry and plasmon surface resonance) were used to screen for interactions between HypA, HypB, UreE and UreG.
RESULTS: Using both methods, affinity constants were found to be 5nM and 13nM for HypA-UreE and 8μM and 14μM for UreG-UreE. Neither Zn(2+) nor Ni(2+) had an effect on the kinetics or stability of the HypA-UreE complex. By contrast, addition of Zn(2+), but not Ni(2+), altered the kinetics and greatly increased the stability of the UreE-UreG complex, likely due in part to Zn(2+)-mediated oligomerization of UreE. Finally our results unambiguously show that HypA, UreE and UreG cannot form a heterotrimeric protein complex in vitro; instead, HypA and UreG compete with each other for UreE recognition. GENERAL SIGNIFICANCE: Factors influencing the pathogen's nickel budget are important to understand pathogenesis and for future drug design.
Copyright © 2012 Elsevier B.V. All rights reserved.

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Year:  2012        PMID: 22698670      PMCID: PMC4017372          DOI: 10.1016/j.bbagen.2012.06.002

Source DB:  PubMed          Journal:  Biochim Biophys Acta        ISSN: 0006-3002


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