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Aleksandra E Sikora1, Suzanne R Lybarger, Maria Sandkvist

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The Vibrio cholerae type II secretion (T2S) system is crucial for outer membrane integrity and pathogen survival. Its disruption causes growth defects and increased sensitivity to harmful agents.

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Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Cell Envelope Structure

Background:

  • The type II secretion (T2S) system in Vibrio cholerae is a complex structure essential for secreting proteins involved in pathogenesis and environmental adaptation.
  • The T2S system spans the bacterial cell envelope, playing a critical role in maintaining cellular functions.

Purpose of the Study:

  • To investigate the consequences of disrupting the T2S system (epsC-N genes) in Vibrio cholerae.
  • To understand the impact on outer membrane integrity, growth, and virulence.

Main Methods:

  • Analysis of a Deltaeps deletion mutant of Vibrio cholerae strain N16961.
  • Assessment of extracellular secretion, growth rates, outer membrane permeability, and stress responses.
  • Evaluation of bacterial survival in a mouse gastrointestinal tract model.
  • Supplementation of culture media with glucose or sucrose to assess phenotypic suppression.

Main Results:

  • Inactivation of T2S genes (epsC-N) led to loss of extracellular secretion and significant growth defects.
  • Outer membrane alterations resulted in increased sensitivity to bile salts and polymyxin B, with periplasmic leakage.
  • The sigma(E) stress response was induced due to T2S system defects.
  • The Deltaeps mutant showed reduced survival in the infant mouse gastrointestinal tract.
  • Supplementation with 5% glucose or sucrose partially suppressed growth defects but did not restore outer membrane integrity.

Conclusions:

  • The T2S system is vital for maintaining Vibrio cholerae's outer membrane barrier function and overall cell envelope integrity.
  • Disruption of the T2S system severely impairs V. cholerae's ability to survive in host environments.
  • Sugars like glucose and sucrose may offer osmoprotection but do not fully rescue the outer membrane defects caused by T2S system inactivation.