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Understanding the Impact of Temperate Bacteriophages on Their Lysogens Through Transcriptomics
Published on: January 5, 2024
Modelling the stability of Stx lysogens
Thomas Evans1, Roger G Bowers, Martin Mortimer
1Department of Mathematical Sciences, Division of Applied Mathematics, Mathematical Sciences Building, The University of Liverpool, Liverpool L69 3BX, UK. t.w.evans@liv.ac.uk
Journal of Theoretical Biology
|July 3, 2007
Summary
Shiga-toxin-converting phages (Stx phages) exhibit a
Area of Science:
- Microbiology
- Molecular Biology
- Computational Biology
Background:
- Shiga-toxin-converting bacteriophages (Stx phages) are temperate phages of Escherichia coli.
- Stx phage lysogen stability is crucial for controlling shiga toxin production and release.
- Stx phage lysogens are known for their instability, often described as a 'hair-trigger' switch to lysis.
Purpose of the Study:
- To investigate if differences in operator regions and repressor binding affinities explain the lower stability of Stx phage lysogens compared to lambda phage.
- To develop a mathematical model for analyzing the molecular switch between lysogeny and lysis in Stx phages.
Main Methods:
- Development of a mathematical model to simulate phage lysogen stability.
- Analysis of operator regions and repressor binding affinities in Stx phages (specifically 933W) and lambda phage.
Main Results:
- The reduced number of binding sites in the Stx phage 933W left operator has minimal impact on lysogen stability.
- Weak repressor binding affinity at the second site in the Stx phage right operator significantly reduces lysogen stability.
- This weak binding affinity may explain the 'hair-trigger' nature of the Stx phage lysogeny-to-lysis switch.
Conclusions:
- Weak repressor binding affinity in the Stx phage right operator is a key factor contributing to reduced lysogen stability.
- The mathematical model provides insights into the behavior and evolution of the phage molecular switch.
- Understanding this switch has implications for managing phage-related diseases and bacterial genome evolution.
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