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Mutations that increase expression of the rpoS gene and decrease its dependence on hfq function in Salmonella

L Brown1, T Elliott

  • 1Department of Microbiology and Immunology, West Virginia University Health Sciences Center, Morgantown 26506, USA.

Journal of Bacteriology
|February 1, 1997
PubMed
Summary
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Host factor I (HF-I) is crucial for RpoS (sigmaS) translation in enteric bacteria. Suppressor mutations bypass HF-I dependence, suggesting RNA secondary structures near the rpoS binding site regulate expression.

Area of Science:

  • Bacteriology
  • Molecular Biology
  • Genetics

Background:

  • RpoS (sigmaS) is a key transcription factor regulating stationary-phase and stress-response genes in enteric bacteria.
  • RpoS also functions as a virulence factor in pathogens like Salmonella typhimurium.
  • Host factor I (HF-I), the product of the hfq gene, is essential for RpoS translation.

Purpose of the Study:

  • To investigate the role of HF-I in RpoS expression.
  • To identify genetic elements that regulate RpoS translation independently of HF-I.

Main Methods:

  • Isolation and characterization of suppressor mutations conferring HF-I independence for rpoS-lac expression.
  • DNA sequencing of suppressor mutations.
  • Genetic analysis to test a proposed model of RNA structure-based regulation.

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Main Results:

  • Suppressor mutations located upstream of rpoS increase rpoS-lac expression without HF-I.
  • Mutations confer significant independence from HF-I.
  • Analysis suggests that RNA secondary structure near the rpoS ribosome binding site regulates translation, with mutations altering this structure.

Conclusions:

  • The findings support a model where RNA secondary structure modulates rpoS mRNA translation.
  • Suppressor mutations likely activate an alternative pathway for RpoS expression, bypassing HF-I.
  • Alternatively, mutations may counteract an HF-I-bound inhibitory element.