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Related Experiment Videos

Excretion of endogenous cadaverine leads to a decrease in porin-mediated outer membrane permeability

H Samartzidou1, A H Delcour

  • 1Department of Biology and Biochemistry, University of Houston, Houston, Texas 77204-5513, USA.

Journal of Bacteriology
|January 28, 1999
PubMed
Summary

Endogenously produced cadaverine, a polyamine, reduces outer membrane permeability in Escherichia coli by inhibiting porin channels. This provides resistance to certain antibiotics and suggests polyamines modulate permeability as an adaptive response.

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • Outer membrane permeability in Escherichia coli is regulated by porin channels.
  • Polyamines are known to inhibit ionic flux through porins.
  • External polyamines affect antibiotic flux, but endogenous effects are less understood.

Purpose of the Study:

  • To investigate the impact of endogenously expressed cadaverine on cephaloridine permeation through porins.
  • To determine if cadaverine acts as an endogenous modulator of outer membrane permeability.

Main Methods:

  • Manipulated the expression of the cadBA operon to control cadaverine levels in Escherichia coli.
  • Measured cephaloridine permeation rates through porins.
  • Assessed changes in porin expression (OmpF, OmpC) and antibiotic resistance.

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Main Results:

  • Increased excreted cadaverine correlated with decreased cephaloridine permeation.
  • Cadaverine-induced porin inhibition was sustained even after polyamine removal.
  • Cells showed resistance to ampicillin but not hydrophobic antibiotics.
  • Expression of cadC alone reduced OmpF and OmpC protein levels.

Conclusions:

  • Endogenously produced cadaverine acts as a sustained inhibitor of porins, reducing outer membrane permeability.
  • Polyamines may serve as endogenous regulators of outer membrane permeability, potentially for adaptation to environmental conditions like acidity.
  • CadC expression influences porin levels, suggesting a novel regulatory mechanism.