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Title: Conversion of the mitochondrial gene for mammalian cytochrome oxidase subunit II to a universal equivalent and expression in E. coli, in vitro, and in Xenopus oocytes
Creator: Cao, Jianli
Date: 1990
Collection: Electronic Theses & Dissertations

Title: Anti-late RNA and transcriptional control in T4 bacteriophage infected Escherichia coli
Creator: Frederick, Robert John, 1944-
Date: 1976
Collection: Electronic Theses & Dissertations

Title: Bioactivities of bovine anti-coliform antibodies elicited by J5 vaccinations
Creator: Chaiyotwittayakun, Anatachai
Date: 2003
Collection: Electronic Theses & Dissertations

Title: Strategies for improving synthesis of quinic acid and shikimic acid from D-glucose
Creator: Jancauskas, Justas
Date: 2008
Collection: Electronic Theses & Dissertations

Title: Deconstructing the correlated nature of ancient and emergent traits : an evolutionary investigation of metabolism, morphology, and mortality
Creator: Grant, Nkrumah Alions
Date: 2020
Collection: Electronic Theses & Dissertations
Description: Phenotypic correlations are products of genetic and environmental interactions, yet the nature of these correlations is obscured by the multitude of genes organisms possess. My dissertation work focused on using 12 populations of Escherichia coli from Richard Lenski's long-term evolution experiment (LTEE) to understand how genetic correlations facilitate or impede an organism's evolution. In chapter 1, I describe how ancient correlations between aerobic and anaerobic metabolism have...
Show morePhenotypic correlations are products of genetic and environmental interactions, yet the nature of these correlations is obscured by the multitude of genes organisms possess. My dissertation work focused on using 12 populations of Escherichia coli from Richard Lenski's long-term evolution experiment (LTEE) to understand how genetic correlations facilitate or impede an organism's evolution. In chapter 1, I describe how ancient correlations between aerobic and anaerobic metabolism have maintained - and even improved - the capacity of E. coli to grow in an anoxic environment despite 50,000 generations of relaxed selection for anaerobic growth. I present genomic evidence illustrating substantially more mutations have accumulated in anaerobic-specific genes and show parallel evolution at two genetic loci whose protein products regulate the aerobic-to-anaerobic metabolic switch. My findings reject the "if you don't use it, you lose it" notion underpinning relaxed selection and show modules with deep evolutionary roots can overlap more, hence making them harder to break. In chapter 2, I revisit previous work in the LTEE showing that the fitness increases measured for the 12 populations positively correlated with an increase in cell size. This finding was contrary to theory predicting smaller cells should have evolved. Sixty thousand generations have surpassed since that initial study, and new fitness data collected for the 12 populations show fitness has continued to increase over this period. Here, I asked whether cell size also continued to increase. To this end, I measured the size of cells for each of the 12 populations spanning 50,000 generations of evolution using a particle counter, microscopy, and machine learning. I show cell size has continued to increase and that it remains positively correlated with fitness. I also present several other observations including heterogeneity in cell shape and size, parallel mutations in cell-shape determining genes, and elevated cell death in the single LTEE population that evolved a novel metabolism - namely the ability to grow aerobically on citrate. This last observation formed the basis of my chapter 3 research where my collaborators and I fully examine the cell death finding and the associated genotypic and phenotypic consequences of the citrate metabolic innovation.
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Title: Coevolution of bacterial-phage interactions
Creator: Meyer, Justin R.
Date: 2012
Collection: Electronic Theses & Dissertations
Description: Bacteria and their viruses, phage, are the most abundant and genetically diverse group of organisms on earth. Given their prevalence, it is no wonder that recent studies have found their interactions important for ecosystem function, as well as the health of humans. Unfortunately, because of technical challenges with studying microbes, some of the most basic questions on their interactions, such as who infects whom, and how their relationships evolved in the first place, remain unanswered....
Show moreBacteria and their viruses, phage, are the most abundant and genetically diverse group of organisms on earth. Given their prevalence, it is no wonder that recent studies have found their interactions important for ecosystem function, as well as the health of humans. Unfortunately, because of technical challenges with studying microbes, some of the most basic questions on their interactions, such as who infects whom, and how their relationships evolved in the first place, remain unanswered. Here I report six studies on bacterial-phage interactions, each focused on understanding their pattern and the underlying biophysical, ecological, and evolutionary processes that shape them. To do this, I tested a number of hypotheses using laboratory experiments and analyses of natural microbial diversity. First, I tested whether Esherichia coli cultured without phage would counter-intuitively evolve new interactions with phage. Typically bacterial traits responsible for phage resistance have pleiotropic consequences on growth, therefore as a side-effect of adapting to an abiotic environment, bacteria may also evolve to become more or less vulnerable to their parasites. After 45,000 generations of laboratory culturing without phage, E. coli gained resistance to lambda phage, gained sensitivity to a mutant T6 phage, and remained resistant to wild type T6. Each response was explained by understanding the pleiotropic costs or benefits of mutations that confer resistance. Because of pleiotropy, interactions may even evolve in the absence of one player.For the rest of my studies I examined how interactions evolve when host and parasite co-occur. First, I found that when E. coli and phage lambda are cocultured, E. coli evolves resistance by reducing the number of phage genotypes that can infect it, whereas, lambda evolves to increase the number of bacterial genotypes it can infect. This antagonism produces a interaction matrix with a nested form where less derived host-ranges fall one within another. To determine whether this nested pattern is an artifact of the labratory environment, or if the pattern is general to natural communities, I performed a metaanalysis on already published phage-bacterial interaction matrices. The majority of networks were significantly nested (28 of 38). Lastly, I examined the molecular basis of E. coli resistance to lambda and found that resistance often evolves through mutations in E. coli's lamB, the gene for the phage receptor. Also, the strength of resistance is correlated with how the mutation perturbs the orientation specific features of the protein structure, primarily loop four which extends out of the cell membrane. For the final two chapters, I studied whether lambda could evolve to target a novel receptor and the evolutionary consequences of such an innovation. Under particular laboratory conditions, E. coli evolves resistance by down-regulating LamB, which sets the stage for lambda to evolve the necessary mutations to exploit a new protein receptor. When allowed to coevolve under this condition, lambda evolved to exploit another outer-membrane protein, OmpF. This new function is the result of a particular combination of four mutations in J, the gene for the protein ligand lambda uses to bind to its host. Once lambda evolves this novel interaction, an evolutionary arms-race begins that drives rapid diversification of the bacteria and phage. Overall, my studies show that coevolution between bacteria and phage, whether it be in the lab or in nature, produces nested interactions matrices. Secondly, antagonistic coevolution is a creative process able to generate new genotypes of host and parasite and promote the evolution of novel function. Lastly, costs for resistance have many important effects, from determining whether resistance will evolve or be lost, to the generation of diversity.
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