Effect of Flik Mutation On The Transcriptional Activity of The Sigma(54) Sigma Factor Rpon In Helicobacter Pylori

Typeset version

 

TY  - JOUR
  - Douillard, Francois P.; Ryan, Kieran A.; Hinds, Jason; O'Toole, Paul W.
  - 2009
  - January
  - Microbiology-SGM
  - Effect of Flik Mutation On The Transcriptional Activity of The Sigma(54) Sigma Factor Rpon In Helicobacter Pylori
  - Validated
  - WOS: 7 ()
  - 155
  - 6
  - 1901
  - 1911
  - Helicobacter pylori is a motile Gram-negative bacterium that colonizes and persists in the human gastric mucosa. The flagellum gene regulatory circuitry of H. pylori is unique in many aspects compared with the Salmonella/Escherichia coli paradigms, and some regulatory checkpoints remain unclear. FliK controls the hook length during flagellar assembly. Microarray analysis of a fliK-null mutant revealed increased transcription of genes under the control of the sigma(54) sigma factor RpoN. This sigma factor has been shown to be responsible for transcription of the class II flagellar genes, including flgE and flaB. No genes higher in the flagellar hierarchy had altered expression, suggesting specific and localized FliK-dependent feedback on the RpoN regulon. FliK thus appears to be involved in three processes: hook-length control, export substrate specificity and control of RpoN transcriptional activity..
  - 1465-2080
  - 10.1099/mic.0.026062-0
DA  - 2009/01
ER  - 
@article{V720668,
   = {Douillard, Francois P. and  Ryan, Kieran A. and  Hinds, Jason and  O'Toole, Paul W.},
   = {2009},
   = {January},
   = {Microbiology-SGM},
   = {Effect of Flik Mutation On The Transcriptional Activity of The Sigma(54) Sigma Factor Rpon In Helicobacter Pylori},
   = {Validated},
   = {WOS: 7 ()},
   = {155},
   = {6},
  pages = {1901--1911},
   = {{Helicobacter pylori is a motile Gram-negative bacterium that colonizes and persists in the human gastric mucosa. The flagellum gene regulatory circuitry of H. pylori is unique in many aspects compared with the Salmonella/Escherichia coli paradigms, and some regulatory checkpoints remain unclear. FliK controls the hook length during flagellar assembly. Microarray analysis of a fliK-null mutant revealed increased transcription of genes under the control of the sigma(54) sigma factor RpoN. This sigma factor has been shown to be responsible for transcription of the class II flagellar genes, including flgE and flaB. No genes higher in the flagellar hierarchy had altered expression, suggesting specific and localized FliK-dependent feedback on the RpoN regulon. FliK thus appears to be involved in three processes: hook-length control, export substrate specificity and control of RpoN transcriptional activity..}},
  issn = {1465-2080},
   = {10.1099/mic.0.026062-0},
  source = {IRIS}
}
AUTHORSDouillard, Francois P.; Ryan, Kieran A.; Hinds, Jason; O'Toole, Paul W.
YEAR2009
MONTHJanuary
JOURNAL_CODEMicrobiology-SGM
TITLEEffect of Flik Mutation On The Transcriptional Activity of The Sigma(54) Sigma Factor Rpon In Helicobacter Pylori
STATUSValidated
TIMES_CITEDWOS: 7 ()
SEARCH_KEYWORD
VOLUME155
ISSUE6
START_PAGE1901
END_PAGE1911
ABSTRACTHelicobacter pylori is a motile Gram-negative bacterium that colonizes and persists in the human gastric mucosa. The flagellum gene regulatory circuitry of H. pylori is unique in many aspects compared with the Salmonella/Escherichia coli paradigms, and some regulatory checkpoints remain unclear. FliK controls the hook length during flagellar assembly. Microarray analysis of a fliK-null mutant revealed increased transcription of genes under the control of the sigma(54) sigma factor RpoN. This sigma factor has been shown to be responsible for transcription of the class II flagellar genes, including flgE and flaB. No genes higher in the flagellar hierarchy had altered expression, suggesting specific and localized FliK-dependent feedback on the RpoN regulon. FliK thus appears to be involved in three processes: hook-length control, export substrate specificity and control of RpoN transcriptional activity..
PUBLISHER_LOCATION
ISBN_ISSN1465-2080
EDITION
URL
DOI_LINK10.1099/mic.0.026062-0
FUNDING_BODY
GRANT_DETAILS