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ScanLag: High-throughput Quantification of Colony Growth and Lag Time
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A long-term epigenetic memory switch controls bacterial virulence bimodality.

Irine Ronin1, Naama Katsowich2, Ilan Rosenshine2

  • 1Racah Institute of Physics, Edmond J. Safra Campus, Faculty of Science, The Hebrew University of Jerusalem, Jerusalem, Israel.

Elife
|February 9, 2017
PubMed
Summary

Enteropathogenic E. coli (EPEC) uses a memory switch to maintain both non-virulent and hyper-virulent states. This phenotypic variability aids colonization and potentially enhances infection spread.

Keywords:
E. coliEPECPerABCbimodal gene expressioncomputational biologyhysteresisinfectious diseasemicrobiologynon-genetic variabilitysystems biologyvirulence regulation

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Area of Science:

  • Microbiology
  • Systems Biology
  • Genetics

Background:

  • Pathogen virulence gene expression is typically activated by environmental cues upon host entry.
  • The transition of pathogens from activating to non-activating conditions and the role of phenotypic variability are not well understood.
  • Variability in virulence gene expression can enhance pathogen colonization during infection.

Purpose of the Study:

  • To systematically investigate the role of phenotypic variability in enteropathogenic E. coli (EPEC) virulence.
  • To understand how EPEC maintains virulence states under both activating and non-activating conditions.

Main Methods:

  • Employed the ScanLag methodology to analyze phenotypic variability in EPEC.
  • Utilized mathematical modeling combined with experimental analysis.
  • Identified key genetic components involved in virulence state switching.

Main Results:

  • Revealed a bimodal growth rate in EPEC populations.
  • Demonstrated that a hysteretic memory-switch mediates this bimodality, allowing stable co-existence of non-virulent and hyper-virulent subpopulations.
  • Identified the 'per' operon as a key component of this hysteretic switch.

Conclusions:

  • EPEC exhibits a unique hysteretic memory switch, enabling the persistence of distinct virulence subpopulations.
  • This mechanism allows EPEC to maintain virulence potential even in non-inducing environments.
  • The identified hysteretic switch may contribute to persistent infections and improved host-to-host transmission.