Effect of MarA-like proteins on antibiotic resistance and virulence in Yersinia pestis

Related Experiment Video

Updated: Jun 19, 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

Ida M Lister1, Joan Mecsas, Stuart B Levy

  • 1Center for Adaptation Genetics and Drug Resistance, Tufts University School of Medicine, Boston, MA 02111, USA.

Infection and Immunity
|October 21, 2009
PubMed

Insights

Two MarA-like proteins in Yersinia pestis significantly impact antibiotic susceptibility and virulence. Deleting these genes reduced multidrug resistance and lung colonization in a pneumonic plague model.

Area of Science:

  • Microbiology
  • Genetics
  • Pathogen Biology

Background:

  • MarA is a transcriptional regulator in Escherichia coli known to influence drug resistance and virulence.
  • Two MarA homologs, MarA47 and MarA48, have been identified in the bacterium Yersinia pestis.
  • Understanding these homologs is crucial for Yersinia pestis pathogenesis research.

Purpose of the Study:

  • To investigate the role of MarA47 and MarA48 in Yersinia pestis.
  • To determine the effect of these proteins on multidrug susceptibility.
  • To assess their contribution to virulence in a pneumonic plague model.

Main Methods:

  • Gene deletion and overexpression of marA47 and marA48 in an attenuated Yersinia pestis strain (KIM 1001 Deltapgm).
  • Assessment of multidrug susceptibility profiles using various antibiotics.
  • Evaluation of lung colonization in a murine model of pneumonic plague.
  • Complementation studies to confirm gene function.

Main Results:

  • Deletion or overexpression of MarA47 or MarA48 altered multidrug susceptibility, including to clinically relevant drugs.
  • Mutants lacking marA47 or marA48 showed a significant, approximately 10-fold decrease in lung colonization.
  • Complementation restored wild-type characteristics, confirming the roles of these genes.

Conclusions:

  • The two MarA homologs in Yersinia pestis, MarA47 and MarA48, are key regulators of antibiotic susceptibility.
  • These homologs play a significant role in the virulence of Yersinia pestis, particularly in lung colonization.
  • Targeting these regulators could be a potential strategy for combating Yersinia pestis infections.

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

Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses08:38

Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses

Published on: February 22, 2019

Related Concept Videos

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...
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...
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...
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...
Clinical Significance of Antibiotic Resistance01:25

Clinical Significance of Antibiotic Resistance

Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...
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,...