Document Detail

Role of the Helicobacter pylori sensor kinase ArsS in protein trafficking and acid acclimation.
MedLine Citation:
PMID:  22865848     Owner:  NLM     Status:  MEDLINE    
Helicobacter pylori survives and grows at low pHs via acid acclimation mechanisms that enable periplasmic pH homeostasis. Important components include a cytoplasmic urease; a pH-gated urea channel, UreI; and periplasmic α-carbonic anhydrase. To allow the rapid adjustment of periplasmic pH, acid acclimation components are recruited to the inner membrane in acid. The ArsRS two-component system, in an acid-responsive manner, controls the transcription of the urease gene cluster and α-carbonic anhydrase. The aim of this study is to determine the role of ArsS in protein trafficking as a component of acid acclimation. H. pylori wild-type and ΔarsS bacteria were incubated at acidic and neutral pHs. Intact bacteria, purified membranes, and total protein were analyzed by Western blotting and urease activity measurements. The total urease activity level was decreased in the ΔarsS strain, but the acid activation of UreI was unaffected. A 30-min acid exposure increased the level and activity of urease proteins at the membrane in the wild type but not in the ΔarsS strain. The urease levels and activity of the ΔarsS strain after a 90-min acid exposure were similar to those of the wild type. ArsS, in addition to its role in urease gene transcription, is also involved in the recruitment of urease proteins to the inner membrane to augment acid acclimation during acute acid exposure. Urease membrane recruitment following prolonged acid exposure in the absence of ArsS was similar to that of the wild type, suggesting a compensatory mechanism, possibly regulated by FlgS, underscoring the importance of urease membrane recruitment and activation in periplasmic pH homeostasis.
Elizabeth A Marcus; George Sachs; Yi Wen; Jing Feng; David R Scott
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.     Date:  2012-08-03
Journal Detail:
Title:  Journal of bacteriology     Volume:  194     ISSN:  1098-5530     ISO Abbreviation:  J. Bacteriol.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-09-26     Completed Date:  2012-12-04     Revised Date:  2013-07-12    
Medline Journal Info:
Nlm Unique ID:  2985120R     Medline TA:  J Bacteriol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5545-51     Citation Subset:  IM    
Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
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MeSH Terms
Acids / toxicity*
Bacterial Proteins / metabolism*
Blotting, Western
Cell Membrane / chemistry
Gene Deletion
Gene Expression Regulation, Bacterial
Helicobacter pylori / chemistry,  genetics,  metabolism,  physiology*
Protein Kinases / genetics,  metabolism*
Protein Transport
Stress, Physiological*
Urease / analysis
Grant Support
Reg. No./Substance:
0/Acids; 0/Bacterial Proteins; EC 2.7.-/Protein Kinases; EC

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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