The HP0256 gene product is involved in motility and cell envelope architecture of <it>Helicobacter pylori</it>

<p>Abstract</p> <p>Background</p> <p><it>Helicobacter pylori </it>is the causative agent for gastritis, and peptic and duodenal ulcers. The bacterium displays 5-6 polar sheathed flagella that are essential for colonisation and persistence in the gastric muco...

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Main Authors: Penn Charles W, Moore Stanley A, Caly Delphine L, Lane Michael C, Ryan Kieran A, Douillard François P, Hinds Jason, O'Toole Paul W
Format: Article
Language:English
Published: BMC 2010-04-01
Series:BMC Microbiology
Online Access:http://www.biomedcentral.com/1471-2180/10/106
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author Penn Charles W
Moore Stanley A
Caly Delphine L
Lane Michael C
Ryan Kieran A
Douillard François P
Hinds Jason
O'Toole Paul W
author_facet Penn Charles W
Moore Stanley A
Caly Delphine L
Lane Michael C
Ryan Kieran A
Douillard François P
Hinds Jason
O'Toole Paul W
author_sort Penn Charles W
collection DOAJ
description <p>Abstract</p> <p>Background</p> <p><it>Helicobacter pylori </it>is the causative agent for gastritis, and peptic and duodenal ulcers. The bacterium displays 5-6 polar sheathed flagella that are essential for colonisation and persistence in the gastric mucosa. The biochemistry and genetics of flagellar biogenesis in <it>H. pylori </it>has not been fully elucidated. Bioinformatics analysis suggested that the gene HP0256, annotated as hypothetical, was a FliJ homologue. In <it>Salmonella</it>, FliJ is a chaperone escort protein for FlgN and FliT, two proteins that themselves display chaperone activity for components of the hook, the rod and the filament.</p> <p>Results</p> <p>Ablation of the HP0256 gene in <it>H. pylori </it>significantly reduced motility. However, flagellin and hook protein synthesis was not affected in the HP0256 mutant. Transmission electron transmission microscopy revealed that the HP0256 mutant cells displayed a normal flagellum configuration, suggesting that HP0256 was not essential for assembly and polar localisation of the flagella in the cell. Interestingly, whole genome microarrays of an HP0256 mutant revealed transcriptional changes in a number of genes associated with the flagellar regulon and the cell envelope, such as outer membrane proteins and adhesins. Consistent with the array data, lack of the HP0256 gene significantly reduced adhesion and the inflammatory response in host cells.</p> <p>Conclusions</p> <p>We conclude that HP0256 is not a functional counterpart of FliJ in <it>H. pylori</it>. However, it is required for full motility and it is involved, possibly indirectly, in expression of outer membrane proteins and adhesins involved in pathogenesis and adhesion.</p>
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spelling doaj.art-c5841496e3604ebea3b14f0b9cb981e02022-12-22T02:58:38ZengBMCBMC Microbiology1471-21802010-04-0110110610.1186/1471-2180-10-106The HP0256 gene product is involved in motility and cell envelope architecture of <it>Helicobacter pylori</it>Penn Charles WMoore Stanley ACaly Delphine LLane Michael CRyan Kieran ADouillard François PHinds JasonO'Toole Paul W<p>Abstract</p> <p>Background</p> <p><it>Helicobacter pylori </it>is the causative agent for gastritis, and peptic and duodenal ulcers. The bacterium displays 5-6 polar sheathed flagella that are essential for colonisation and persistence in the gastric mucosa. The biochemistry and genetics of flagellar biogenesis in <it>H. pylori </it>has not been fully elucidated. Bioinformatics analysis suggested that the gene HP0256, annotated as hypothetical, was a FliJ homologue. In <it>Salmonella</it>, FliJ is a chaperone escort protein for FlgN and FliT, two proteins that themselves display chaperone activity for components of the hook, the rod and the filament.</p> <p>Results</p> <p>Ablation of the HP0256 gene in <it>H. pylori </it>significantly reduced motility. However, flagellin and hook protein synthesis was not affected in the HP0256 mutant. Transmission electron transmission microscopy revealed that the HP0256 mutant cells displayed a normal flagellum configuration, suggesting that HP0256 was not essential for assembly and polar localisation of the flagella in the cell. Interestingly, whole genome microarrays of an HP0256 mutant revealed transcriptional changes in a number of genes associated with the flagellar regulon and the cell envelope, such as outer membrane proteins and adhesins. Consistent with the array data, lack of the HP0256 gene significantly reduced adhesion and the inflammatory response in host cells.</p> <p>Conclusions</p> <p>We conclude that HP0256 is not a functional counterpart of FliJ in <it>H. pylori</it>. However, it is required for full motility and it is involved, possibly indirectly, in expression of outer membrane proteins and adhesins involved in pathogenesis and adhesion.</p>http://www.biomedcentral.com/1471-2180/10/106
spellingShingle Penn Charles W
Moore Stanley A
Caly Delphine L
Lane Michael C
Ryan Kieran A
Douillard François P
Hinds Jason
O'Toole Paul W
The HP0256 gene product is involved in motility and cell envelope architecture of <it>Helicobacter pylori</it>
BMC Microbiology
title The HP0256 gene product is involved in motility and cell envelope architecture of <it>Helicobacter pylori</it>
title_full The HP0256 gene product is involved in motility and cell envelope architecture of <it>Helicobacter pylori</it>
title_fullStr The HP0256 gene product is involved in motility and cell envelope architecture of <it>Helicobacter pylori</it>
title_full_unstemmed The HP0256 gene product is involved in motility and cell envelope architecture of <it>Helicobacter pylori</it>
title_short The HP0256 gene product is involved in motility and cell envelope architecture of <it>Helicobacter pylori</it>
title_sort hp0256 gene product is involved in motility and cell envelope architecture of it helicobacter pylori it
url http://www.biomedcentral.com/1471-2180/10/106
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