The ability of traits to adapt in response to change is one of the most fundamental aspects of evolution. Optimality models used to predict adaptation frequently make simplifying assumptions about the ability of traits to evolve freely within simple tradeoffs. However, we frequently have little understanding of genomic mechanisms underlying phenotypic evolution. Genetic constraints clearly limit phenotypic change, but the extent to which they do so is unclear. I will explore molecular and phenotypic responses to genomic and environmental perturbations through experimental evolution in T7 bacteriophage. First, I studied evolutionary robustness of the lysis time phenotype when lysin gene lysozyme was deleted. This deletion profoundly delayed lysis and thus decreased fitness. Evolved phages recovered much of the lost fitness and mostly restored lysis timing. The recovery was mediated by changes in a tail fiber gene (gene 16) with muralytic activity that is generally used in genome entry. Next, I extended the work on lysozyme to observe the effect of increasing constraint on evolutionary recovery. The effects of various combinations of deletions of lysozyme, 17.5 (which plays a role in lysis) and 16 suggested that another gene played a role similar to 17.5 in lysis. The phage defective in both lysozyme and 16 did not lyse hosts thoroughly even after long periods of infection, suggesting that these were the only effective lysin genes. Adaptation of this phage on cells expressing the essential gp16 constrained the primary adaptive pathway of recovery from lysozyme deletion. A mutually exclusive alternative pathway involving a variety of different genes evolved. The line recovered the ability to lyse normal hosts, by a mechanism involving multiple mutations. Finally, I tested the ability of T7 to adapt to an optimum lysis time. Based on empirical results from other phages, mature phage virions accumulate linearly inside the cell over time. This assumption underlies a model suggesting that availability of hosts determines optimal lysis time. While adaptation to different host densities caused the expected qualitative evolutionary changes, adaptation to conditions expected to select for slow lysis did not lead to the quantitative optimum. This is probably due to nonlinear virion accumulation.
| Identifer | oai:union.ndltd.org:UTEXAS/oai:repositories.lib.utexas.edu:2152/3439 |
| Date | 28 August 2008 |
| Creators | Heineman, Richard Hugh, 1978- |
| Contributors | Bull, James J. |
| Source Sets | University of Texas |
| Language | English |
| Detected Language | English |
| Type | Thesis |
| Format | electronic |
| Rights | Copyright © is held by the author. Presentation of this material on the Libraries' web site by University Libraries, The University of Texas at Austin was made possible under a limited license grant from the author who has retained all copyrights in the works. |
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