Journal of Molecular Evolution

, Volume 61, Issue 2, pp 181–191

Evolutionary Robustness of an Optimal Phenotype: Re-evolution of Lysis in a Bacteriophage Deleted for Its Lysin Gene

  • Richard H. Heineman
  • Ian J. Molineux
  • James J. Bull
Article

DOI: 10.1007/s00239-004-0304-4

Cite this article as:
Heineman, R.H., Molineux, I.J. & Bull, J.J. J Mol Evol (2005) 61: 181. doi:10.1007/s00239-004-0304-4

Abstract

Optimality models are frequently used to create expectations about phenotypic evolution based on the fittest possible phenotype. However, they often ignore genetic details, which could confound these expectations. We experimentally analyzed the ability of organisms to evolve towards an optimum in an experimentally tractable system, lysis time in bacteriophage T7. T7 lysozyme helps lyse the host cell by degrading its cell wall at the end of infection, allowing viral escape to infect new hosts. Artificial deletion of lysozyme greatly reduced fitness and delayed lysis, but after evolution both phenotypes approached wild-type values. Phage with a lysis-deficient lysozyme evolved similarly. Several mutations were involved in adaptation, but most of the change in lysis timing and fitness increase was mediated by changes in gene 16, an internal virion protein not formerly considered to play a role in lysis. Its muralytic domain, which normally aids genome entry through the cell wall, evolved to cause phage release. Theoretical models suggest there is an optimal lysis time, and lysis more rapid or delayed than this optimum decreases fitness. Artificially constructed lines with very rapid lysis had lower fitness than wild-type T7, in accordance with the model. However, while a slow-lysing line also had lower fitness than wild-type, this low fitness resulted at least partly from genetic details that violated model assumptions.

Keywords

Optimality Experimental evolution Evolutionary robustness Lysis T7 Bacteriophage Genome evolution Molecular evolution Fitness Adaptation 

Copyright information

© Springer Science+Business Media, Inc. 2005

Authors and Affiliations

  • Richard H. Heineman
    • 1
  • Ian J. Molineux
    • 2
    • 3
  • James J. Bull
    • 1
    • 3
  1. 1.Section of Integrative BiologyUniversity of TexasAustinUSA
  2. 2.Section of Molecular Genetics and MicrobiologyUniversity of TexasAustinUSA
  3. 3.Institute for Cell and Molecular BiologyUniversity of TexasAustinUSA

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