The human polycore minisatellite probes 33.6 and 33.15 developed by Prof. Alec Jeffreys and colleagues have been shown to detect hypervariable minisatellites in many taxonomically dispersed species. The mRNA derivatives of these two probes, pSPT19.6 and pSPT18.15, have here been used to probe the genomes of four species currently maintained in captivity. The wild populations of these species, Rothschild's mynah, the Rodrigues fruit bat, the British Merlin and the New Zealand falcon, are threatened with extinction to varying degrees. By using the technique of DNA fingerprinting, it has been possible to assess the levels of minisatellite variation remaining in these stocks, to confirm or refute the parent/offspring allocations made within, and in the case of Rothschild's mynah, to demonstrate that at least two of the founders of the stock were closely related. In addition, it has been possible to show that there is a significant positive relationship between the similarity coefficient calculated between two adults and the inbreeding coefficient calculated for their offspring.

No description available.

This thesis is an attempt to reconstruct the physical environment of the Port Phillip area as it was at the time of first European arrival, ie. c.1800. At the time it was first encountered by Europeans, in 1803, the land around Port Phillip Bay supported a wide diversity of ecosystems. For millennia the area was the territory of Aboriginal clans belonging to two language groups, Woi wurrung and Boon wurrung. These peoples lived in spiritual union with the land, exploiting its abundant resources, and, through a range of practices, maintaining it in the form in which it had been created. The encroachment of Europeans onto clan estates, beginning in the 1830s, brought dramatic changes to this Aboriginal way of life, and also to the local landscapes themselves. The thesis propounded here is that the natural history of the area was a major influence on the occupation and use of the area by humans, and that to understand the particulars of that natural history is to have an insight into the human history. The bulk of the study is therefore a reconstruction of that natural history, which is offered as the physical context of human action in the area. (For complete abstract open document)

Thesis (M.A.) in Liberal Studies--University of Maine, 2001. / Includes vita. Includes bibliographical references (leaves 83-85).

Thesis (M.A.)--Oregon State University, 2008. / Printout. Includes bibliographical references (leaves 143-152). Also available on the World Wide Web.

Within the UK, the continuing biodiversity crisis has led to a policy driven shift in the conservation sector; moving away from localized site scale conservation to a landscape-scale. This approach encourages fragmented habitat patches to be integrated into a much larger habitat network. Epiphytic lichens provide an ideal model system for studying the effectiveness of conservation initiatives within fragmented habitats, due to their metapopulation structures whereby individual trees within woodlands (and woodland stands within wooded landscapes), represent isolated habitat patches. Old-growth woodland in particular provides suitable habitat to a suite of lichens known as the Lobarion community, which are declining throughout Europe. Regeneration within these old growth areas, though essential for future habitat persistence, causes shading and ultimately leads to local extinctions of shade intolerant lichen epiphytes. A landscape scale conservation strategy that relies on habitat permeability to balance colonisation of post-regeneration woodland patches with extinctions in ageing woodland patches elsewhere in the landscape has been proposed as a management strategy to meet the needs of both lichen epiphytes and their woodland habitat. The unique conditions found in western Scotland, combining a relative abundance of high quality old growth habitat (in a European context) coupled with robust populations of some members of the Lobarion community, could provide an ideal opportunity to test such a management strategy. In this thesis, the plausibility of landscape-scale conservation as a management strategy for epiphytic lichens is explored, using a suite of nine target epiphytes of contrasting ecological traits set within Glen Creran, a temperate rainforest on the west coast of Scotland: 1. The habitat requirements of nine target epiphytes were identified and predictions of species distribution made over an entire glen using a species distribution modelling (SDM) approach. The SDM’s were found to apply more generally within the wider biogeographic area for five of the nine species, providing an evidence base for future conservation plans in Scotland’s rainforest zone. 2. A novel method to determine dispersal distance in lichen epiphytes was developed, combining a mechanized propagule trap with molecular techniques. This methodological advance allowed the first direct comparative study of lichen epiphytes in a natural context. 3. An agent based model was developed combining the results of 1. and 2. above to investigate the effect of habitat connectivity on colonisation in six contrasting lichen epiphytes, enabling inferences of species response to landscape-scale conservation scenarios within the study system to be made.

In this project I explore the development of bird illustrations in early American natural history publication. I follow three groups in Philadelphia from 1812 to 1858: institutions, artist-naturalists, and printmakers. Each of these groups modeled a certain normative vision of illustration, promoting, producing, and publishing images that reflected their senses of what constituted good illustration. I argue that no single set of actors in this narrative did work that would become the ultimate standard-bearer for ornithological illustration; rather, all of them negotiated the conflicting interests of their own work as positioned against, or alongside, those who had come before. Their diverse intentions, aesthetic and practical, sat prominently in their separate visions of drawing birds; utility, artistry, and feasibility of the images directed the creation of the illustrations. How they used their ideal ways of depicting birds changed the ways that their successors would confront the practice of illustrating birds. / Master of Science

As sessile organisms, plants had to develop various biochemical and physiological mechanisms to respond and adapt to abiotic stress conditions such as salt and drought and thus acquire stress tolerance. A particular interesting mechanism is the so called “priming effect”: an application of a mild short stress to plants at an early stage of development appears to enable them to cope better when stressed again at mature stage. However, the molecular effects of salt priming have not been systematically quantified and as a consequence the molecular basis of priming remains unknown. In this study an experimental procedure was established that allowed to test whether salt priming of young Arabidopsis thaliana plants had an effect on plants exposed to more severe salt stress at a later stage of development. To quantify how primed and non-primed plants responded to the second salt stress, global changes in their transcriptional expression profiles were monitored using Affymetrix GeneChip ATH1 microarray. Results showed that both primed and non-primed plants responded to the salt treatment modulating the same set of known stress responsive genes. However, primed plants differentially regulated a smaller set of genes. Furthermore, the vast majority of the stress responsive genes showed a weaker response in primed than in nonprimed plants. These results suggested that primed plants channelled the stress response using only selected genes. The next question addressed was how primed plants could “remember” the priming treatment after a period of extensive growth. Several studies had indicated that environmental stress induces changes in the chromatin structure thereby modifying the accessibility of the DNA for transcription factors and other regulatory proteins. This suggested a link between epigenetic modification and exposure of plants to stressful conditions, where the chromatin status might act as an epigenetic mark that could be maintained during plant growth and development. To investigate this hypothesis I carried out a comparative analysis of the epigenetic landscapes of primed and non-primed plants combining Chromatin Immuno-Precipitation with Illumina sequencing (ChIP-Seq). Genome-wide profiles of H3K4me2, H3K4me3, H3K9me2 and H3K27me3 were generated for roots and shoots of plants harvested immediately after the priming treatment. Roots of primed plants showed indeed numerous differences in their epigenetic profiles compared to non-primed roots, in particular at the level of H3K27me3. Therefore, I carried out an additional ChIP-Seq experiment before the application of the second stress to test if the priming induced changes in H3K27me3 were maintained over this period of extensive growth. Results showed that several epigenetic differences caused by priming were still maintained. Finally, to elucidate the relationship between epigenetic modifications and transcriptional responses the ChIP-Seq profiles were coupled with genome wide transcript profiles obtained by RNA-seq. Results shown that in the non-steady state there was no clear correlation between the differences detected at the transcriptional and at the epigenetic level. The results identified H3K27me3 as a potential mark for salt stress memory and they call for future studies extending both temporal and spatial resolution of epigenetic and transcriptional changes after salt priming.

It is estimated that there are approximately 1030 ocean virioplankton (Suttle 2007; Parsons et al. 2012). A large component of the oceanic viriosphere are the cyanophages, viruses that specifically infect cyanobacteria. Recent advances in genomics has revealed such viruses encode a multitude of genes, often acquired horizontally, that act to redirect metabolism for their own gains (Mann et al. 2003; Lindell et al. 2004a; Millard et al. 2009; Sullivan et al. 2010; Hurwitz et al. 2013; Enav et al. 2014). These genes have been named auxiliary metabolic genes (AMGs). They include multiple subunits of complexes involved with photosynthetic electron transport (PET) and CO2 fixation (Mann et al. 2003; Lindell et al. 2004; Millard et al. 2009; Sullivan et al. 2010; Thompson et al. 2011; Puxty et al. submitted), leading to the hypothesis that cyanophages directly participate in photosynthesis to provide carbon and energy for their own replication. Cyanophages face a dynamically changing light environment during their rather lengthy infection cycles ~12hrs. Therefore, it was hypothesised that changes in light intensity may affect the physiology of phage infection in terms of photosynthesis, CO2 fixation and infection dynamics. During infection of the marine cyanobacterium Synechococcus sp. WH7803 with the well characterised cyanophage S-PM2 I show that decoupling of the photochemical and CO2 fixation reactions of photosynthesis occurs (Chapter 3), which presumably redirects metabolism towards energy generation and away from growth. Moreover, S-PM2 acts to modify the PET which results in improved functioning of PSII at HL. The result is that the lytic cycle is significantly shortened during infection of the Synechococcus host under HL compared with low light (LL) conditions. To understand whether this early lysis is a regulated process, whole transcriptome sequencing of S-PM2 was performed in HL and LL (Chapter 5). This revealed a general increase in expression of all genes in HL but only the cyanophage psbA gene was significantly up-regulated above this background. This AMG encodes a core complex of photosystem II (PSII) of the PET and therefore plays a vital role in supplying energy through photophosphorylation. It is concluded that light poses a metabolic constraint on cyanophage development that requires large amounts of energy for synthesis and assembly of the structural components of the virion. Cyanophages have therefore acquired and evolved coordinated expression of PSII genes to maintain this supply of energy. I further hypothesise that gene expression may pose a significant barrier in the acquisition of AMGs from their host due to incompatible gene regulation. To test this, the phage transcriptome was analysed (Chapter 4) to validate the model of temporal transcriptional regulation in cyanophage S-PM2 as previously proposed by comparison to enterobacteriophage T4. It is shown that the experimental data is largely congruent with the proposed model. This also revealed unpredicted characteristics of the transcriptome, including genome wide transcriptional read-through and antisense expression. It is suggested that this is facilitated by either inefficient transcriptional termination or pervasive transcription initiation and may be a biologically relevant process that allows for moderate expression of recently acquired genes. In addition, genome-wide antisense transcription may act to regulate the inventory or temporal expression of specific mRNAs in these regulatory limited phages. Attempts were therefore made to characterise a previously detected non-coding RNA (ncRNA) antisense to the light regulated S-PM2 psbA gene (Chapter 6). A model is proposed suggesting that the asRNA may act to tweak psbA expression under LL conditions to prevent accumulation of unnecessary PSII proteins. This mechanism has an interesting effect on the rate of splicing of a group I intron encoded by the psbA gene. This study provides an important leap forward in our understanding of the factors that regulate the infection dynamics and therefore ecology of cyanophages. In so doing it also reveals transcriptional constraints and adaptations that go some way to explaining the evolution of cyanophage genomes.

This thesis is divided into two main chapters. The first chapter relates to studies undertaken to gain insights into the mechanism of action on liver growth by the peroxisome proliferator (PP) ciprofibrate and the chemical cyproterone acetate (CPA) in rodents. Peroxisome proliferators are a class of chemicals that have diverse effects in rats and mice including increased DNA synthesis and peroxisome proliferation. Peroxisome proliferators include herbicides, plasticisers, hypolipidemic drugs and synthetic fatty acids. These chemicals act through ligand activation of nuclear membrane receptors termed ‘peroxisome-proliferator-activated receptors’ (PPARs), which ultimately activate nuclear transcription. PPs induce a cellular process in liver characterised by dramatic increases in the size and number of peroxisomes, correlated with both hepatocyte hypertrophy (i.e. an increase in the size of liver cells) and hyperplasia (i.e. an increase in the number of liver cells during replicative DNA synthesis and cell division). However, the mechanism of action of increased hepatocyte growth is not currently understood. Understanding the mechanism by which increased liver growth is induced by PPs in rodents will hopefully provide insights into how natural liver growth occurs and might have medical benefits for human health if the mechanism of PP toxicity can be overcome. Knowledge gained from the mechanism of PP activation might also then be applied to other chemical carcinogens. Therefore, firstly the mode of action of the peroxisome proliferator ciprofibrate was investigated. Previous work had indicated that two successive doses of ciprofibrate treatment separated by 24hr led to two rounds of liver cell replication, but it was not clear whether the same or different hepatocytes were involved in this growth response. To study this phenomenon, histochemical experimental work was undertaken to assess whether the same or different hepatocyte cells were stained during the two rounds of cell division following ciprofibrate treatment. The two histochemical stains used were EdU and BrdU, which are both base-pair analogues that stain nuclei undergoing DNA replication. It was hypothesized that if EdU was used to stain cells at 24 hr and then BrdU at 48 hr, that if the same cells were responding to ciprofibrate treatment then cells would be co-stained by both dyes, whereas if different cells were responding then there would be little or no double staining of hepatocyte cells. It was found that different cells were stained by the two dyes, indicating that ciprofibrate treatment was targeting different cells. Secondly, the mode of action of the carcinogen cyproterone acetate (CPA) on hepatocyte growth was investigated. Previous work had investigated the effects of CPA on hepatocyte growth in male and female rats and had suggested differences in response between the sexes. In the present study female rats were treated with CPA, to assess whether differences in labelling indices were present compared to previous male results. Female F-344/NHsd rats, aged 14-15 weeks, were treated with CPA and then injected with BrdU at 22 hr, and rats were killed 2 hr later. Results confirmed that the female rats had a considerably higher labelling index (50%) compared to male rats (6%). This suggested that upregulation of gene expression in female rats was much higher, which might provide an exciting opportunity to identify sets of genes involved in carcinogenic responses. To investigate whether there was any overlap between genes induced by ciprofibrate and CPA treatment a preliminary study was designed where female rats were gavaged with CPA and then killed 3 hr later. Real-time PCR analysis of a small number of target genes showed no consistent changes in expression between the present CPA and previous ciprofibrate treatment results, suggesting largely different modes of action of these chemicals. The second chapter of this thesis relates to studies undertaken to gain insights into neurodegenerative disorders. Neurodegeneration is a gradual loss of structure or function of neurons, which may lead to neuronal death. Neurodegenerative diseases including Parkinson’s, Alzheimer’s, and Huntington’s occur as a result of neurodegenerative changes. Several studies have suggested that PPARs have critical roles in reducing the brain inflammation which in turn might have a significant effect on reducing the fundamental processes involved. Work was performed using a mouse model of dementia with lewy body disease (Psmc1fl/fl; CaMKIIα-Cre) to represent neurodegenerative disorder, and involved parallel, in vivo and in vitro investigations to determine whether the development of neurodegenerative diseases occurs at the same rate in vitro and in vivo i.e. a comparison of rapidity of pathogenicity progression was made. Astrocytes were used to track the development of disease, given that these play a key role in neurological disorders, using an immunohistochemistry approach. A PPAR-γ analogue was used to investigate the role of PPARs in reducing astrocytes proliferation. To optimise the validity of the results, four controls were used including an antagonist T0070907 which abolished the effect of rosiglitazone treatment alone. The results on the effect of PPAR-γ agonist and rosiglitazone, after a week of treatment, showed that the PPAR-γ agonist inhibited astrocytes activation in both the cortex and hippocampus of the mutant mice organotypic slice culture. The number of GFAP +ve astrocytes was significantly decreased in mutant mice with 100 µM rosiglitazone in both areas, whereas 50 µM rosiglitazone showed a decrease in the number of astrocytes in the cortex, but the effect was less in the region of the hippocampus. This finding suggests that PPs such as rosiglitazone may have potential uses as therapeutic drugs to inhibit neurodegeneration.