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Biophys. J. BioFAST: First Published June 20, 2008. doi:10.1529/biophysj.108.133694
© 2008 by the Biophysical Society.


A more recent version of this article appeared on September 15, 2008.
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BIOPHYSICAL THEORY AND MODELING

Collective decision making in bacterial viruses

Joshua S Weitz 1*, Yuriy Mileyko 1, Richard I Joh 1 and Eberhard O Voit 1

1 Georgia Institute of Technology

* To whom correspondence should be addressed. E-mail: jsweitz{at}gatech.edu.

Submitted on March 17, 2008
Revised on April 14, 2008
Accepted on 16 May 2008


   Abstract
For many bacterial viruses, the choice of whether to kill host cells or enter a latent state depends on the multiplicity of coinfection. Here, we present a mathematical theory of how bacterial viruses can make collective decisions concerning the fate of infected cells. We base our theory on mechanistic models of gene regulatory dynamics. Unlike most previous work, we treat the copy number of viral genes as variable. Increasing the viral copy number increases the rate of transcription of viral mRNAs. When viral regulation of cell fate includes nonlinear feedback loops, very small changes in transcriptional rates can lead to dramatic changes in steady state gene expression. Hence, we prove that deterministic decisions can be reached, e.g., lysis or latency, depending on the cellular multiplicity of infection within a broad class of gene regulatory models of viral decision making. Comparisons of a parametrized version of the model with molecular studies of the decision structure in the temperate bacteriophage {lambda} are consistent with our conclusions. Because the model is general, it suggests that bacterial viruses can respond adaptively to changes in population dynamics, and that features of collective decision making in viruses are evolvable life history traits.

Key Words: bacteriophage lambda, gene regulation, lysis, lysogeny, nonlinear dynamics







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Copyright © 2008 by the Biophysical Society.