Posttranscriptional Regulation of Flagellin Synthesis In Helicobacter Pylori By The Rpon Chaperone Hp0958

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TY  - JOUR
  - Douillard, FP, Ryan, KA, Caly, DL, Hinds, J, Witney, AA, IIusain, SE, O'Toole, PW
  - 2008
  - August
  - Journal of Bacteriology
  - Posttranscriptional Regulation of Flagellin Synthesis In Helicobacter Pylori By The Rpon Chaperone Hp0958
  - Validated
  - ()
  - 190
  - 24
  - 7975
  - 7984
  - The Helicobacter pylori protein HP0958 is essential for flagellum biogenesis. It has been shown that HP0958 stabilizes the sigma(54) factor RpoN. The aim of this study was to further investigate the role of HP0958 in flagellum production in H. pylori. Global transcript analysis identified a number of flagellar genes that were differentially expressed in an HP0958 mutant strain. Among these, the transcription of the major flagellin gene flaA was upregulated twofold, suggesting that HP0958 was a negative regulator of the flaA gene. However, the production of the FlaA protein was significantly reduced in the HP0958 mutant, and this was not due to the decreased stability of the FlaA protein. RNA stability analysis and binding assays indicated that HP0958 binds and destabilizes flaA mRNA. The HP0958 mutant was successfully complemented, confirming that the mutant phenotype described was due to the lack of HP0958. We conclude that HP0958 is a posttranscriptional regulator that modulates the amount of the flaA message available for translation in H. pylori..
  - DOI 10.1128/JB.00879-08
DA  - 2008/08
ER  - 
@article{V722037,
   = {Douillard,  FP and  Ryan,  KA and  Caly,  DL and  Hinds,  J and  Witney,  AA and  IIusain,  SE and  O'Toole,  PW },
   = {2008},
   = {August},
   = {Journal of Bacteriology},
   = {Posttranscriptional Regulation of Flagellin Synthesis In Helicobacter Pylori By The Rpon Chaperone Hp0958},
   = {Validated},
   = {()},
   = {190},
   = {24},
  pages = {7975--7984},
   = {{The Helicobacter pylori protein HP0958 is essential for flagellum biogenesis. It has been shown that HP0958 stabilizes the sigma(54) factor RpoN. The aim of this study was to further investigate the role of HP0958 in flagellum production in H. pylori. Global transcript analysis identified a number of flagellar genes that were differentially expressed in an HP0958 mutant strain. Among these, the transcription of the major flagellin gene flaA was upregulated twofold, suggesting that HP0958 was a negative regulator of the flaA gene. However, the production of the FlaA protein was significantly reduced in the HP0958 mutant, and this was not due to the decreased stability of the FlaA protein. RNA stability analysis and binding assays indicated that HP0958 binds and destabilizes flaA mRNA. The HP0958 mutant was successfully complemented, confirming that the mutant phenotype described was due to the lack of HP0958. We conclude that HP0958 is a posttranscriptional regulator that modulates the amount of the flaA message available for translation in H. pylori..}},
   = {DOI 10.1128/JB.00879-08},
  source = {IRIS}
}
AUTHORSDouillard, FP, Ryan, KA, Caly, DL, Hinds, J, Witney, AA, IIusain, SE, O'Toole, PW
YEAR2008
MONTHAugust
JOURNAL_CODEJournal of Bacteriology
TITLEPosttranscriptional Regulation of Flagellin Synthesis In Helicobacter Pylori By The Rpon Chaperone Hp0958
STATUSValidated
TIMES_CITED()
SEARCH_KEYWORD
VOLUME190
ISSUE24
START_PAGE7975
END_PAGE7984
ABSTRACTThe Helicobacter pylori protein HP0958 is essential for flagellum biogenesis. It has been shown that HP0958 stabilizes the sigma(54) factor RpoN. The aim of this study was to further investigate the role of HP0958 in flagellum production in H. pylori. Global transcript analysis identified a number of flagellar genes that were differentially expressed in an HP0958 mutant strain. Among these, the transcription of the major flagellin gene flaA was upregulated twofold, suggesting that HP0958 was a negative regulator of the flaA gene. However, the production of the FlaA protein was significantly reduced in the HP0958 mutant, and this was not due to the decreased stability of the FlaA protein. RNA stability analysis and binding assays indicated that HP0958 binds and destabilizes flaA mRNA. The HP0958 mutant was successfully complemented, confirming that the mutant phenotype described was due to the lack of HP0958. We conclude that HP0958 is a posttranscriptional regulator that modulates the amount of the flaA message available for translation in H. pylori..
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DOI_LINKDOI 10.1128/JB.00879-08
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