This thesis is a comparative study of gene arrangements in Pseudomonas species, and is organized into three major sections. The first section compares gene arrangements for different pathways in Pseudomonas aeruginosa PAO1 to determine if the gene arrangements are similar to previous studies. It also serves as a reference for pyrimidine gene arrangements in P. aeruginosa. The second part compares the physical, and genetic maps of P. aeruginosa PAO1 with the genome sequence. The final section compares pyrimidine gene arrangements in three species of Pseudomonas. Pyrimidine biosynthesis and salvage genes will be aligned for P. aeruginosa PAO1, P. putida KT2440, and P. syringae DC3000. The whole study will gives insight into gene patterns in Pseudomonas, with a focus on pyrimidine genes.

Endosymbiosis in arthropods involves intracellular bacteria that supply an array of benefits to the host. Endosymbionts likely enhance the health of ticks by provisioning amino acids such as cysteine and tyrosine, and cofactors such as biotin and folic acid that are not available in blood--the sole nutrient source of ticks. Endosymbionts of ticks are of special interest due to their close evolutionary relationship with tick-vectored pathogens that impact livestock and human health. For example, ticks typically contain Coxiella-like endosymbionts (CLEs) that are the closest relatives of the human pathogen Coxiella burnetii. In order to understand the evolutionary relationship between the mammalian pathogen Francisella tularensis, which is vectored by ticks, and the Francisella-like endosymbionts (FLEs) present in several ticks, we assembled the genomes of the FLEs in the hard tick Amblyomma maculatum and the soft tick Ornithodoros moubata using high-throughput sequencing. While this project was in progress, another group described the genome of an FLE in the soft tick Argus (Persicargas) arboreus. Utilizing the three genomes, we show that all FLEs evolved from a mammalian pathogen, a relationship that is converse to that of C. burnetii, which likely evolved from a tick-associated non-pathogenic ancestor. Additionally, our analyses indicate that FLEs are horizontally transferred between ticks, and due to their superior metabolic capabilities could replace ancestral endosymbionts with reduced genomes.

Bibliography: leaves 363-381.

Bibliography: leaves 363-381. / ix, 381 leaves : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Molecular Biosciences, 2002

Thesis (M. Phil.)--University of Hong Kong, 2007. / Title proper from title frame. Also available in printed format.

Thesis (Ph. D.)--Oregon State University, 2007. / Printout. Includes bibliographical references. Also available on the World Wide Web.

Vibrio vulnificus is an opportunistic human and animal pathogen that is predominantly found in estuarine waters. In aquatic ecosystems, it colonizes filter-feeders, such as oysters, and has been found to form biofilms on the surface of various marine organisms, including plankton, algae, fish, eels, and crustaceans. The bacterium can spontaneously develop a rugose phenotype, which is associated with the production of polysaccharide(s) that impart a raised, wrinkled appearance to cells, copious biofilm formation, and increased stress resistance. Biofilm and rugose colony development, along with pellicle and aggregate formation, are believed to be crucial for the environmental survival and persistence of V. vulnificus. As the biosynthesis of polysaccharide(s) is a key feature linking these physiological processes, the main objectives of this study were to identify polysaccharide loci contributing to survival phenotypes in V. vulnificus and to gain insight into the regulation of these loci. Two polysaccharide loci (brp and rbd) were found to contribute to biofilm formation. The brp locus is regulated by the second messenger c-di-GMP and by at least two transcriptional regulators BrpR and BrpT. Lesions in glycosyltransferases in the locus or in either of the regulators abated the inducing effects of c-di-GMP on biofilm formation. The rbd locus is regulated not by c-di-GMP, but instead by a response regulator (RbdG) belonging to the TCRS family, which is encoded within the locus. The biofilms associated with the expression of the brp and rbd polysaccharides were structurally unique and simultaneous expression of both loci dramatically enhanced pellicle formation. Each locus also provides unique survival characteristics; the development of rugosity and stress resistance could be attributed to brp expression whereas rbd expression augmented aggregate formation. The ability of V. vulnificus to differentially regulate expression of the brp and rbd polysaccharides may allow the bacterium to “fine tune” its biofilm lifestyle to maximally benefit from the characteristics associated with each locus.

Vibrio vulnificus is an opportunistic human and animal pathogen that is predominantly found in estuarine waters. In aquatic ecosystems, it colonizes filter-feeders, such as oysters, and has been found to form biofilms on the surface of various marine organisms, including plankton, algae, fish, eels, and crustaceans. The bacterium can spontaneously develop a rugose phenotype, which is associated with the production of polysaccharide(s) that impart a raised, wrinkled appearance to cells, copious biofilm formation, and increased stress resistance. Biofilm and rugose colony development, along with pellicle and aggregate formation, are believed to be crucial for the environmental survival and persistence of V. vulnificus. As the biosynthesis of polysaccharide(s) is a key feature linking these physiological processes, the main objectives of this study were to identify polysaccharide loci contributing to survival phenotypes in V. vulnificus and to gain insight into the regulation of these loci. Two polysaccharide loci (brp and rbd) were found to contribute to biofilm formation. The brp locus is regulated by the second messenger c-di-GMP and by at least two transcriptional regulators BrpR and BrpT. Lesions in glycosyltransferases in the locus or in either of the regulators abated the inducing effects of c-di-GMP on biofilm formation. The rbd locus is regulated not by c-di-GMP, but instead by a response regulator (RbdG) belonging to the TCRS family, which is encoded within the locus. The biofilms associated with the expression of the brp and rbd polysaccharides were structurally unique and simultaneous expression of both loci dramatically enhanced pellicle formation. Each locus also provides unique survival characteristics; the development of rugosity and stress resistance could be attributed to brp expression whereas rbd expression augmented aggregate formation. The ability of V. vulnificus to differentially regulate expression of the brp and rbd polysaccharides may allow the bacterium to “fine tune” its biofilm lifestyle to maximally benefit from the characteristics associated with each locus.

Thesis (Ph. D.)--University of Queensland, 2002. / Includes bibliographical references.

Thesis (M. Phil.)--University of Hong Kong, 2002. / Includes bibliographical references (leaves 119-135).