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With global climates changing rapidly, animals must adapt to new environmental conditions with altered weather and phenology. Key to adapting to these new conditions is adjusting the timing of reproduction to have offspring when the conditions are best to maximize growth and survival. Using a long-term dataset on a wild population of yellow-bellied marmots (Marmota flaviventer) at the Rocky Mountain Biological Laboratory (RMBL), we investigated how the timing of reproduction changed with changing spring conditions over the past 50 years. Marmots are hibernators with a four-month active season. It is thus crucial to reproduce early enough in the season to have time to prepare for hibernation, but not too early so as snow cover prevents access to food. Importantly, climate change in this area has increased spring temperatures by 5 °C and decreased spring snowpack by 50 cm over the past 50 years. This directional change in climate may have caused adaptation. Given that adaptation to environmental conditions could arise from either microevolution or phenotypic plasticity, we evaluated how female marmots adjust the timing of their reproduction and estimated the importance of both genetic variance and plasticity in the variation in this timing. We show that, within a year, the timing of reproduction is not as tightly linked to the date a female emerges from hibernation as previously thought. We report a positive effect of spring snowpack but not of spring temperature on the timing of reproduction. There is inter-individual variation in the timing of reproduction but not in its response to changing spring conditions. Genetic variance in the timing of reproduction is low, and heritability was 8%. Earlier pup emergence date increases the number and weighted proportion of pups surviving their first winter, indicative of directional selection on this trait. The same pattern is not found for litter size with no effect of pup emergence date on the number of pups born. Further, all three of these traits are not under stabilizing selection. Taken together, it seems that we should expect some changes in this population with changing climatic conditions, but because of plasticity and not due to natural selection. Further, future studies on the marmots should not operate under the assumption that females reproduce immediately following their emergence.

Biofouling is the accumulation of sessile marine organisms, such as algae, tube worms and barnacles on man-made substrata and has negative economic and ecological implications. Ship hulls are readily fouled, which significantly increases drag while decreasing ship fuel efficiency when moving through water. Fouled hulls have also become important vectors of invasive species. These problems are minimized when hulls are painted with a toxic anti-fouling or non-toxic foul-release coating. Due to recent restrictions of anti-fouling paint use, research and development of non-toxic alternatives has increased. Novel hull coating efficiency is often quantified by the critical removal stress value of barnacles from the coating. Barnacle adhesive cement protein content is thought to be responsible for barnacles’ incredible ability to adhere underwater. The expression level and type of adhesive proteins has eluded scientists due to their extreme insolubility within cured barnacle cement. Identification of these proteins may provide insight to the adhesion of fouling species and aid coating development. Barnacles are a cosmopolitan organism, able to withstand a wide range of environmental conditions, yet foul-release coating research had not previously incorporated environmental factors as variables in determining coating performance. Temperature is known to affect protein structure and function and is also a formative factor of barnacle larvae survival and development. Even so, the interaction between temperature and barnacle adhesion to has not previously been explored. We examined the effect of temperature on barnacle adhesion to foul-release coatings. After observing differences in critical removal stress due to temperature, we attempted to attribute these differences to specific proteins within the adhesive using 2D SDS PAGE. Gel image analysis determined that there were significant differences in cement protein expression between barnacles raised within different temperatures. Preliminary protein identification with Mass Spectronomy (MALDI TOF/TOF) was performed, however further research and a larger barnacle genomic database is needed to elucidate barnacle cement protein sequences.

Anthropogenic impacts to the environment are unavoidable currently; however, my research investigates a potential mitigation method for amphibians dealing with poor health outcomes caused by detrimental anthropogenic changes to their wetlands. Environmental stressors such as antibiotics leeching from manure of domesticated farm animals into local wetlands can cause a dysbiosis of the gastrointestinal bacterial flora within tadpoles. Dysbiosis of gastrointestinal bacteria during early tadpole development is associated with a decrease in development rate, decrease in body mass accumulation, and other poor health outcomes. I investigated if increasing the indigestible fiber (prebiotic) content in wood frog tadpole’s alfalfa based diet could return tadpoles with stripped microbiomes (dysbiotic gastrointestinal bacterial community composition) to the same phenotype of healthy control tadpoles. I also did a pilot study to see if diet could help in increasing survival post infection with Ranavirus, and from both studies, I created NGSS aligned curriculum and activities. I found that a 10% corn starch enriched alfalfa diet significantly increased the body mass accumulation and development rate of stripped tadpoles. I found there was an association with metabolism and gut dysbiosis. Unfortunately, the connection in regards to corticosterone release was unclear. There was an association with diet and survival, but it needs to be repeated with a larger sample size.

<p>Theories that engender fundamental transformations in our world view seldom come perfect from the outset for two reasons. First, the empirical discoveries and theoretical framework necessary for their full explanatory efficacy are often not yet in place. Secondly, as a consequence of the first, some of the auxiliary theories and assumptions they rely upon are often antiquated and erroneous. For these reasons, anomalies are frequent in scientific theories. In this thesis, I discuss some of the major scientific anomalies, including particularly, the paradox of altruism. I suggest that the paradox of altruism arises because one of the most fundamental Mendelian genetic principles is misapplied. I show that today’s explanatory models err in supposing altruism and selfishness to be genetic allelomorphs. The supposition is inconsistent with the field data on altruism, and entails a logical inconsistency in accounting for the evolution of altruism. Largely, the models that purport to resolve the paradox hinge on the conditional expression of the altruistic gene, a move which I argue contradicts the theoretical assumption that engenders the paradox in the first place. I demonstrate from the empirical data that altruism and selfishness are rather plastic phenotypic expressions of a single genotype. And by supplanting the standard neo-Darwinian assumptions with the principle of phenotypic plasticity, I provide a parsimonious account of the evolution and maintenance of altruism which entails no paradox.</p> / Master of Arts (MA)

For animals at high altitude, low oxygen (hypoxia) is an unremitting stressor that has the potential to impair metabolism and performance. The hypoxic chemoreflex senses reductions in the partial pressure of O2 in the arterial blood and thus elicits many of the physiological responses to hypoxia, including increases in breathing and activation of the sympathetic nervous system. The hypoxic chemoreflex is vital to surviving acute exposure to severe hypoxia, but the advantage of this reflex during chronic hypoxia is less clear. The goals of my thesis were to examine how control of breathing by the hypoxic chemoreflex has evolved in high-altitude natives to maintain O2 transport in chronic hypoxia, and to elucidate the potential genetic mechanisms that were involved. This was accomplished using deer mice (Peromyscus maniculatus) native to high- and low-altitudes, in addition to a strictly low-altitude species (P. leucopus). I found that high-altitude deer mice breathe with higher total ventilation using preferentially deeper breaths, contributing to higher O2 saturation of arterial blood, but in contrast to lowland mice highlanders do not exhibit ventilatory plasticity in response to chronic hypoxia. These phenotypes appeared to be uniquely evolved in the highland population and arise during the onset of endothermy in early post-natal development. I then used second-generation inter-population hybrids to evaluate the effects of genetic variation (specifically, in the hypoxia-inducible factor 2a gene Epas1 and in haemoglobin genes) on an admixed genomic background. The high-altitude variant of α-globin could completely explain the deep breathing pattern of highland mice, whereas the high-altitude variant of Epas1 and possibly β-globin contributed to their apparent lack of ventilatory plasticity in response to chronic hypoxia. Together, the physiological changes elicited by these mutations contribute to maintaining O2 uptake and metabolism in the cold and hypoxic environment at high altitude. / Thesis / Doctor of Philosophy (PhD) / High-altitude environments are amongst the harshest on earth, with extremely low levels of oxygen, but some animals not only survive but thrive in these conditions. How these animals do so was previously not well understood. My thesis has uncovered how the evolution of respiratory physiology contributes to high-altitude adaptation in the deer mouse, the species with the broadest altitudinal distribution of any North American mammal, and has elucidated the genetic mechanisms involved. My work contributes to understanding nature’s solutions to oxygen deprivation – an all too common problem in many human and animal diseases.

Individuals within a single population can vary widely in their phenotype e.g. in their body shape. These differences are an important source of biodiversity and they can precede evolutionary divergence within a population. In this thesis we use the biological invasion of the zebra mussels into Swedish lakes to investigate which processes create or maintain phenotypic diversity within populations of the two native fish species perch and roach and the mussel itself. Both fishes have specially adapted body shapes that depend on whether they feed in the near-shore or open-water habitat of lakes. This habitat-specific divergence was more pronounced in lakes with zebra mussels, probably because resources in both habitats were in higher supply due to the mussels’ effects on the lakes. Divergence in perch body shapes between habitats was also higher in lakes with a higher water clarity, suggesting that visual conditions can affect the resource use and thus also the expression of a habitat-specific body shape. When investigating the diversity of body shapes in the mussel itself we found that mussels from one lake changed their shell shape when exposed to different predators: fish predators induced a more elongated shell shape while crayfish predators induced a rounder shell. These specific shell shapes probably serve as two alternative predator defenses protecting the mussel from predation. We conclude that the availability and use of distinct resources is an important source of diversity within populations. Abiotic conditions can play a previously underappreciated role by promoting or impairing the use of the distinct resources thus affecting the divergence. The diversity of shell shapes we found in the zebra mussels complements our study by demonstrating that not only consumer responses to resources but also resources’ responses to predators can generate phenotypic diversity.

Rhabdomyosarcoma (RMS) is a type of soft tissue sarcoma that mainly occurs in children. RMS can be divided into two subtypes embryonal (ERMS) and alveolar (ARMS). The ARMS subtype can be especially aggressive when a balanced chromosomal translocation is present. This translocation results in the expression of a PAX3/7-FOXO1 fusion protein, an oncogenic transcription factor. PAX3-FOXO1 positive RMS has an especially bad prognosis and survival rate. In the cell painting assay relevant organelles are stained and morphological features are extracted on a cellular level. Based on these features, morphological profiles of each cell type and a similarity score can be calculated. The morphological profiles of ERMS cell lines RD and RD18 as well as the ARMS cell lines RH30 and CW9019 were obtained. RD and RD18 are most similar to each other followed by RH30. CW9019 has a very different profile from the other cell lines. Since ERMS is associated with a better survival rate a drug that reprograms the phenotype from ARMS to a more ERMS-like phenotype might sensitize the cells to the standard treatment of RMS. ARMS patients might then benefit from a combination therapy of such a drug and the standard treatment. To find such a drug a drug screen was conducted. Drugs were selected for the screen that either target fusion-protein stability or overexpressed targets of the fusion protein. Phenotypic reference compounds were included to get a first idea of the mechanisms and involved organelles of the screened drugs. In total, 30 compounds and 9 phenotypic reference compounds were screened for changing morphological profiles of RMS cell lines with the cell painting assay. 15 compounds were identified that change the phenotype of the ARMS cell line RH30. In addition, 7 of these compounds shift the phenotype of RH30 towards an ERMS-like phenotype. If that morphological resemblance of RH30 cells to ERMS cells translates into a change of a more ERMS-like behavior and sensitizes the cells for the standard treatment of RMS remains to be investigated. The reprogramming hits showed high similarity with phenotypic reference compounds that increase nucleus size which might suggest changed behavior of the fusion protein. Especially, Bosutinib, Midostaurin and Alisertib are promising new compounds for ARMS treatment. They shifted the ARMS phenotype towards an ERMS-like phenotype in the drug screen. This shift is likely a result of the interaction with PLK1 or Aurora-kinase A that are shown to have an influence on fusion-protein stability.

Small but mighty phytoplankton can be used as excellent model organisms to answer questions that are of importance to marine biologists and researchers in experimental evolution alike. For example, marine biologists are interested in finding out, how, in a changing ocean, the phytoplankton foundation of the ocean ecosystem is going to change - can we use short-term data to extrapolate to longer timescales? What are the physiological consequences of selection in stable and fluctuating high-pCO2 environments? From a more evolutionary perspective, is elevated pCO2 alone enough to drive evolution in marine algae? Can we select organisms to maintain plasticity in fluctuating environments, and how does selection in a fluctuating environment affect their ability to evolve? Can we detect a cost of plasticity? I have used theoretical and practical approaches from both disciplines to answer these questions, as they are ultimately similar questions that are important to address, and the lack of communication between disciplines has lead to conflicting predictions on the fate of populations in changing environments. Using evolutionary theory and applying it to an organism with a known function in the marine environment allows us to make ecologically relevant predictions while also enabling us to disentangle the underlying evolutionary mechanisms. While there have been some studies focusing on evolution of marine algae in climate change scenarios since I started my PhD, my study is the first to test the link between phenotypic plasticity and adaptation empirically, and it is also the first to use 16 rather than single or few genotypes of an algae, thereby creating the statistical power necessary to make any predictions. In a short-term CO2 enrichment study, and a selection experiment, those 16 physiologically and genetically distinct lineages of Ostreococcus, the smallest free living eukaryote, were selected for 400 generations in fluctuating and stable high pCO2 environments. I have shown that short-term plastic responses in phenotype can predict the magnitude of long-term evolutionary ones. Ostreococcus lineages in fluctuating environments evolve to be more plastic with no associated costs, and the adaptive response to selection in a high pCO2 environment is to grow more slowly in monoculture, but to be more successful competitors in mixed culture. High-pCO2 evolved lineages are genetically and physiologically different from their ancestors. Importantly, their quality as a food source for zooplankton will change, with possible repercussions for the ocean ecosystem at a whole. Furthermore, the lineages’ ability to perceive pCO2 levels in the surrounding medium is altered after evolution in fluctuating and high pCO2 environment, allowing them to broaden the window in which they can respond to changes in their environment without suffering metabolic stress.

Unprecedented rates of anthropogenic environmental change have resulted in dramatic decreases in biodiversity worldwide. In order to persist during changes in both the abiotic and biotic environment resulting from anthropogenic stressors such as climate change and habitat degradation, populations must be able to respond or face extirpation. Predicted population-level responses to environmental change include i) range shifts as individuals disperse into more suitable regions, ii) phenotypic plasticity allowing for shifts in the mean phenotype of the population or iii) microevolution resulting from a genetic change within the population. The goal of this thesis is to assess how species within a community respond to a dramatic change in the environment. This study used the sediment record of a Subarctic pond to investigate the impacts of a rapid increase in salinity on two species of the crustacean zooplankton Daphnia. One species, Daphnia tenebrosa, was unable to persist in the high salinity conditions and is believed to have been extirpated from the system. The other species, Daphnia magna, was tolerant of the new environmental conditions and was present throughout the sediment record. To investigate the changes in life history of D. magna, resting eggs from the sediment were hatched to compare iso-female lines from pre- and post-disturbance time periods. No differences were observed between the clone lines, suggesting that phenotypic plasticity allowed D. magna to persist despite the rapidly changing environmental conditions, and that microevolution in salinity tolerance may not have occurred in this population. This study suggests that, in environments with moderate levels of post environmental change, pre-existing phenotypic plasticity may play a greater role than microevolution in species response to environmental changes. However, not all species from a community display the same response to environmental changes, as seen in this study with the extirpation of D. tenebrosa. To better understand how communities will be affected by future environmental change, further investigations need to be made on what factors influence species response. Identifying species response may allow conservation efforts to focus on species that are unlikely to adapt to environmental change, and are most at risk. / Thesis (Master, Biology) -- Queen's University, 2013-09-29 21:54:34.881