Phenotypic plasticity, the ability of a genotype to express different phenotypes in different environments, allows organisms to cope with variation in resources and invade novel environments. Biologists have long been fascinated with the costs and tradeoffs that generate and maintain variation in plasticity, such as possible increases in brain size and delays in reproduction associated with the evolution of learning. However, the costs of plasticity vary: many studies have failed to find costs of plasticity, the degree of costs often vary with the system or environments considered, and many costs of plasticity are variable even within the lifetime of an individual. This research adopts a developmental perspective to predict the degree and incidence of costs of plasticity, using host learning in butterflies as a case study. Learning, a mechanism of plasticity that develops through a trial-and-error sampling process, should result in developmental costs and allocation of energy towards development (at the expense of reproduction). Furthermore, costs of learning should be less pronounced in environments for which organisms have innate biases and for learned traits underlain by short-term memory, relative to long-term memory (which requires more developmental re-structuring). This research found support for all three predictions across three levels of costs: behavioral costs, tissue costs, and fecundity trade-offs. Butterflies exhibited genetic variation in their ability to learn to recognize different colored hosts. Genotypes with higher proxies for long-term memory emerged with relatively larger neural investment and smaller reproductive investment. In contrast to these costs of long-term learning, proxies of short-term learning were only correlated with increased exploration of a range of possible resources (types of non-hosts) early in the host-learning process. Family-level costs of plasticity emerged from the ability to learn to locate a red host, for which butterflies do not have an innate bias. Costs of learning were also induced by learning itself: following exposure to novel (red) host environments, individual butterflies, regardless of genetic background, increased exploratory behavior, increased neural investment, and re-allocated energy away from reproduction towards other functions (e.g., flight). Considering developmental mechanisms helps to predict how costs will influence the evolution of learning and plasticity.

Sonoran Desert Drosophila mettleri breeds in soil soaked by the necrotic cacti juices from saguaro (Carnegiea gigantea) and cardon (Pachycereus pringlei). An isolated population on Santa Catalina Island, 300 kilometers NW of the Sonoran Desert limit, was discovered breeding in several Opuntia cacti species. Host shifts are associated with the speciation process in phytophagous insects. I tested for evidence of premating isolation, postmating isolation, and ecological differences among allopatric populations of Drosophila mettleri using a variety of approaches. No sexual isolation was detected. However, Drosophila mettleri from Santa Catalina Island shows significant behavioral and physiological differences compared with Sonoran Desert populations. Furthermore, Drosophila mettleri from Santa Catalina Island was significantly genetically differentiated from all other populations in the study. Finally, I observed sufficiently significant F1 male sterility in crosses involving the Santa Catalina Island population to consider it indicative of early postzygotic isolation.

Mouse Hepatitis virus (MHV) is a member of the coronavirus family in the order Nidovirales. The 32 kb genome contains cis-acting sequences necessary for replication of the viral genome. Those cis-acting sequences have been shown to bind host proteins, and binding of those proteins is necessary for virus replication. One of the cis-acting elements is the 3' terminal 42 nucleotide host protein binding element. Previous work has demonstrated that mitochondrial aconitase, mitochondrial heat shock protein 70, heat shock protein 60 and heat shock protein 40 bind to the 3' terminal 42 nucleotide host protein binding element. We demonstrated that RNA secondary structure of the 3' terminal 42 nucleotide host protein binding element is necessary for host protein binding in vitro. We also demonstrate that primary structure of the 3' terminal 42 nucleotide host protein binding element is necessary for viral replication by targeted recombination. DI replication assays infer that the 3' terminal 42 nucleotide host protein binding element plays a role in positive strand synthesis from the negative strand template. Current studies involve the infectious cDNA clone, which will provide definitive answers on the role of the 3' terminal 42 nucleotide host protein binding element in MHV replication.

The present study proposes a significant role for host country nationals (HCNs) in the expatriate adjustment process. Based on self-categorizaton theory, newcomer socialization research, organizational citizenship behavior (OCB) research, and models of expatriate adjustment, I present a model proposing how social categorization processes influence HCNs' willingness to engage in adjustment-facilitating organizational citizenship behaviors (AOCBs). I further propose that these behaviors have a significant impact on expatriates' adjustment and in turn, other important job-related outcomes of the expatriate. Hypotheses were tested on 115 expatriates and 53 HCNs. Expatriates were contacted directly or via an organizational contact. HCNs were either contacted directly or nominated by their expatriate counterpart to participate in the study. Results reveal support for the main tenets of the model. The willingness to engage in AOCBs was related to outgroup categorization, collectivism, and perceptions of justice. Social support provided by HCNs was found to significantly relate to HCNs' perceptions of their expatriate co-worker's adjustment. Expatriates, however, indicated that spousal adjustment and language ability were more important for their own adjustment. Adjustment was related to other key expatriate outcomes. The research and managerial implications of these results are discussed.

Whiteflies (Bemisia tabaci, Biotype B, Homoptera: Aleyrodidae) are pests of cotton crops, affecting the yield of the crop both indirectly and directly. These pests feed on the leaves of cotton plants and produce "honeydew," a sticky liquid excretion which covers the lint of the open cotton boll creating problems during the processing of the lint. High densities of these pests also can decrease the productivity of the cotton plant by stripping it of vital nutrients. The primary objective of this research was to screen 116 converted cotton race stocks for resistance to sweetpotato whiteflies. Responses of converted race stocks to whiteflies are compared to that of known susceptible commercial cultivars PSC 355 and Delta Pearl. Screens for antibiosis resistance to whitefly were established using excised leaves placed in a nutrient solution (¼ strength Hoagland's). Cohort populations of whiteflies were established on these leaves and followed daily to determine differences in developmental time as well as percent survival. Resistant candidates were determined using a chi-squared test comparing the ranked sums of leaf averages for the two selection criteria, whitefly developmental time and percent whitefly survival, of each cotton race stock to that of the putative known susceptibles (KS). These tests showed 6 converted race stocks to be significantly different (P ≤ 0.1) from the KS for at least one of the two selection criteria. Of these converted race stocks, M-9044-0154 and M-9044-0156 showed to have lower whitefly survival than the KS, while M-9644-0188, M-9644-0195, M-0044-0221, and M-9644-0242 showed whitefly to have an increased developmental time. Retesting of these six converted race stocks along with several others identified another race stock line, M-0044-0171, which was significantly different from the KS. Retesting also indicated that M-9644-0188 was different for survival in addition to developmental time which was determined in the original screening. Additional tests were conducted in the greenhouse and field to examine these race stock lines. Greenhouse screenings indicated that M-9044-0156 and M-9644-0188 contained possible non-preference resistance characteristics. Field screenings conducted in Weslaco and College Station, TX in 2002 and 2003 failed to provide useful data due to low densities of insects.

Emerging infectious diseases, pollution and climate change are associated with amphibian extinction events worldwide; however, direct causation is often obscured by the interactions of these stressors. Elucidating the possible synergies between metal contamination and disease is, therefore, critical in advancing our knowledge of the co-evolutionary mechanisms in host-pathogen systems and helping with the ability to better forecast the spread of diseases in metal-stressed environments. Additionally, increasing ecotoxicological research has improved our understanding of the complex influence trace metals may have on the physico-chemical nature of aquatic systems; however, the discrepancy in concentration-response within the toxicological literature makes it difficult to accurately define the range of toxicity, often due to the variability in media used in experimentation. The first chapter of this thesis reports an evaluation of copper, nickel and copper/nickel concentrations on several Northern Leopard Frog (Lithobates [Rana] pipiens) larvae life history traits within field collected smelting effluent water. Overall, results indicated that copper had a stronger negative impact on survival than nickel. However, tadpoles exposed to copper displayed increased growth and developmental patterns while those exposed to nickel demonstrated opposing life history traits. These results indicate that tadpoles are displaying different fitness strategies, in terms of survival and life history, in the presence of increased copper and/or nickel stress.

The emergence of pathogens resistant to available drug therapies is a pressing global health problem. Antimicrobial peptides (AMPs) may potentially form new therapeutics to counter these pathogens. AMPs are key components in the mammalian innate immune system and are responsible for both direct killing and immunomodulatory effects in host defense against pathogenic organisms. This thesis describes computational methods for the identification of novel natural and synthetic AMPs. A bioinformatic resource was constructed for classification and discovery of gene- coded AMPs, consisting of a database of clustered known AMPs and a set of hidden Markov models (HMMs). One set of 146 clusters was based on the mature peptide sequence, and one set of 40 clusters was based on propeptide sequence. The bovine genome was analyzed using the AMPer resources, and 27 of the 34 known bovine AMPs were identified with high confidence and up to 69 AMPs were predicted to be novel peptides. One novel cathelicidin AMP was experimentally verified as up-regulated in response to infection in bovine intestinal tissue. A chemoinformatic analysis was performed to model the antibacterial activity of short synthetic peptides. Using high-throughput screening data for the activities of over 1400 peptides of diverse sequence, quantitative structure-activity relation (QSAR) models were created using artificial neural networks and physical characteristics of the peptide that included three-dimensional atomic structure. The models were used to predict the activity of a set of approximately 100,000 peptide sequence variants. After ranking the predicted activity, the models were shown to be very accurate. When 200 peptides were synthesized and screened using four levels of expected activity, 94% of the top 50 peptides expected to have the highest level of activity were found to be highly active. Several promising candidates were synthesized with high quality and tested against several multi- antibiotic-resistant pathogens including clinical strains of Pseudomonas aeruginosa, Staphylococcus aureus, Enterococcus faecalis and Escherichia coli. These peptides were found to be highly active against these pathogens as determined by minimal inhibitory concentration; this serves as independent confirmation of the effectiveness of high-throughput screening and in silico analysis for identifying peptide antibiotic drug leads.

The cationic host defence peptide LL-37 is an immunomodulatory agent that plays an important role in epithelial innate immunity. Previously, concentrations of LL-37 thought to represent levels present during inflammation have been shown to elicit the production of cytokines and chemokines by epithelial cells. To investigate the potential of lower concentrations of LL-37 to alter epithelial cell responses, normal primary keratinocytes and bronchial epithelial cells were treated with pro-inflammatory stimuli in the presence or absence of 1 – 3 μg/ml LL-37. Low, physiologically relevant concentrations of LL-37 synergistically increased IL-8 production by both proliferating and differentiated keratinocytes in response to IL-1β and the TLR5 agonist flagellin, and synergistically increased IL-8 production by bronchial epithelial cells in response to IL-1β, flagellin, and the TLR2/1 agonist PAM3CSK4. Treatment of bronchial epithelial cells with LL-37 and the TLR3 agonist poly(I:C) resulted in synergistic increases in IL-8 release and cytotoxicity. The synergistic increase in IL-8 production observed when keratinocytes were co-stimulated with flagellin and LL-37 was suppressed by pretreatment with inhibitors of Src-family kinase signalling and NF-κB translocation. These data suggest that low concentrations of LL-37 may alter epithelial responses to microbes in vivo. Microarray analysis of keratinocyte transcriptional responses after LL-37 treatment suggest that LL-37 may alter the expression of growth factors and a number of genes important to innate immune responses. LL-37 may thus play a more important role than previously suspected in the regulation of epithelial inflammation; an improved understanding of the mechanisms by which LL-37 alters chemokine responses could lead to the development of novel anti-infective and anti-inflammatory therapeutics.

Hepatitis C virus (HCV) is a serious global health problem with an estimate of 170 million carriers worldwide. Most individuals exposed to this blood-borne pathogen develop chronic infection, which may result in severe liver complications as well as end-stage liver diseases including cirrhosis and hepatocellular carcinoma. Current treatment options are suboptimal with no effective vaccines available to date. Development of a readily accessible mouse model that is permissive to natural HCV infection is important to facilitate drug and vaccine discovery, and also to better understand the viral pathogenesis. The inherent difficulty is that HCV displays very limited tropism, infecting only livers from humans or chimpanzees. An attempt was made to elucidate the key determinants in rendering the murine intracellular environment permissive to HCV replication. The results revealed that deletion of the interferon regulatory factor-3 and overexpression of microRNA-122 can independently enhance viral subgenomic replication in murine fibroblasts, with microRNA-122 being the stronger determinant. Interestingly, the phenotype established by these genetic manipulations was insufficient to support full-length HCV genome replication. Murine hepatic cell lines, with or without microRNA-122 expression, were also non-permissive to genomic HCV replication, despite the fact that translation of viral RNA was observed. These results suggest that additional host-specific factor(s) are required to support replication of full-length HCV RNA. These studies provide insight on the essential factors capable of influencing permissiveness of rodent cells to HCV replication, and also suggest genetic modifications to be considered when modeling the complete viral life cycle in a rodent animal model.

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