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Related Experiment Video

Updated: Aug 28, 2025

Design and Use of a Low Cost, Automated Morbidostat for Adaptive Evolution of Bacteria Under Antibiotic Drug Selection
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Growth-mediated negative feedback shapes quantitative antibiotic response.

S Andreas Angermayr1,2, Tin Yau Pang3,4, Guillaume Chevereau5

  • 1Institute for Biological Physics, University of Cologne, Cologne, Germany.

Molecular Systems Biology
|September 20, 2022
PubMed
Summary
This summary is machine-generated.

Antibiotic trimethoprim’s weak effect on bacterial growth stems from a feedback loop where slower growth increases the drug target, dihydrofolate reductase (DHFR). This mechanism could be used to combat antibiotic resistance.

Keywords:
antibioticsdihydrofolate reductase (DHFR)dose-response curvefeedback loopsresource allocation model

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Area of Science:

  • Microbiology
  • Systems Biology
  • Pharmacology

Background:

  • Dose-response relationships quantify biological system responses to stimuli.
  • Antibiotic dose-response curves are crucial for treatment and resistance evolution but their underlying mechanisms are unclear.
  • Trimethoprim exhibits a uniquely shallow dose-response curve in bacteria.

Purpose of the Study:

  • To elucidate the mechanisms behind trimethoprim's shallow dose-response curve in Escherichia coli.
  • To investigate the role of growth-mediated feedback in antibiotic efficacy.
  • To explore the potential of manipulating feedback loops for antimicrobial drug design.

Main Methods:

  • Quantitative analysis of bacterial growth and antibiotic effects.
  • Molecular characterization of drug target (dihydrofolate reductase) expression.
  • Genetic manipulation of feedback pathways.
  • Mathematical modeling of cellular resource allocation and growth dynamics.

Main Results:

  • A negative growth-mediated feedback loop explains trimethoprim's shallow dose-response curve.
  • Trimethoprim-induced growth inhibition leads to upregulation of its target, dihydrofolate reductase (DHFR).
  • DHFR upregulation is a general response to growth rate, not specific to trimethoprim.
  • Altering the feedback loop predictably modifies the dose-response curve.

Conclusions:

  • Growth-mediated feedback loops significantly shape antibiotic dose-response relationships.
  • The identified feedback mechanism offers a potential target for novel antimicrobial strategies.
  • Exploiting these feedback loops could lead to evolutionary traps that select against drug resistance.