Related Experiment Video

Updated: Jun 23, 2026

Quantifying Yersinia pseudotuberculosis Type III Secretion System Activity Following Iron Starvation and Anaerobic Growth
08:36

Quantifying Yersinia pseudotuberculosis Type III Secretion System Activity Following Iron Starvation and Anaerobic Growth

Published on: May 31, 2024

An iron-regulated LysR-type element mediates antimicrobial peptide resistance and virulence in Yersinia

Sonia Arafah1,2,3,4, Marie-Laure Rosso3,1,2,4, Linda Rehaume5

  • 1Inserm U801, F-59019 Lille, France.

Microbiology (Reading, England)
|April 25, 2009
PubMed

Insights

Yersinia pseudotuberculosis uses a gene (YPTB0333) to regulate iron uptake and resist antimicrobial peptides. This gene is essential for the bacterium to colonize host tissues during infection.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Molecular Biology

Background:

  • Entero-invasive bacteria like Yersinia pseudotuberculosis face challenges such as iron starvation and antimicrobial compounds during host infection.
  • Previous research indicated that Yersinia pseudotuberculosis grown in iron-deprived conditions exhibit increased resistance to the antimicrobial peptide polymyxin B.

Purpose of the Study:

  • To identify the genetic basis for polymyxin B resistance observed in iron-deprived Yersinia pseudotuberculosis.
  • To elucidate the regulatory role of the identified gene in bacterial adaptation and virulence.

Main Methods:

  • Genetic analysis to identify the responsible gene (YPTB0333) encoding a LysR family transcriptional regulator.
  • Gene expression analysis to determine the targets regulated by YPTB0333.
  • In vivo mouse model of oral infection to assess the role of YPTB0333 in colonization.

Main Results:

  • The YPTB0333 gene was identified as the mediator of polymyxin B resistance under iron-limiting conditions.
  • YPTB0333 acts as a pleiotropic regulator, controlling its own expression, the Yfe iron-uptake system, and polymyxin B resistance.
  • YPTB0333 is crucial for Yersinia pseudotuberculosis colonization of Peyer's patches and mesenteric lymph nodes in a mouse infection model.

Conclusions:

  • YPTB0333 plays a significant role in Yersinia pseudotuberculosis virulence by coordinating iron acquisition and antimicrobial resistance.
  • The regulation of iron uptake and resistance by YPTB0333 is critical for successful colonization of host tissues.

More Related Videos

Analysis of Yersinia enterocolitica Effector Translocation into Host Cells Using Beta-lactamase Effector Fusions12:23

Analysis of Yersinia enterocolitica Effector Translocation into Host Cells Using Beta-lactamase Effector Fusions

Published on: October 13, 2015

Imaging InlC Secretion to Investigate Cellular Infection by the Bacterial Pathogen Listeria monocytogenes14:05

Imaging InlC Secretion to Investigate Cellular Infection by the Bacterial Pathogen Listeria monocytogenes

Published on: September 19, 2013

Related Concept Videos

Regulation of Bacterial Virulence01:28

Regulation of Bacterial Virulence

Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...
Plague01:24

Plague

Plague is a highly virulent zoonotic disease caused by Yersinia pestis, a Gram-negative, facultatively anaerobic coccobacillus. This pathogen primarily circulates among rodent populations and is transmitted to humans through the bite of infected fleas. Additional transmission routes include direct contact with infected animal tissue or inhalation of respiratory droplets from individuals with pneumonic plague. These multiple transmission pathways highlight the bacterium’s potential for rapid...
Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...
Development of Antibiotic Resistance01:30

Development of Antibiotic Resistance

Antibiotic resistance is a major public health concern that arises when bacteria evolve mechanisms to withstand the effects of antibiotic treatments. This resistance can be intrinsic, acquired through genetic mutations, or transferred between bacteria via horizontal gene transfer. The development of antibiotic resistance poses significant challenges in treating bacterial infections and necessitates ongoing research to develop new therapeutic strategies.Intrinsic resistance occurs when bacterial...
Mechanism of Antibiotic Resistance in MRSA01:25

Mechanism of Antibiotic Resistance in MRSA

Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
Stringent Response in E. coli01:23

Stringent Response in E. coli

Bacterial growth is closely tied to nutrient availability, with cells proliferating exponentially under favorable conditions and entering a stationary phase when resources become scarce. This transition is mediated by a regulatory mechanism known as the stringent response, which allows bacteria to adapt to nutrient deprivation by modulating gene expression and metabolic activity.During nutrient scarcity, intracellular amino acid levels decline. It results in the accumulation of uncharged tRNAs...