School of BioSciences - Theses
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ItemThe effects of artificial light at night on the behaviour and physiology of Drosophila melanogaster( 2019)Artificial light at night is one of the most pervasive and least recognised anthropogenic pollutants. Its extent and intensity is expanding globally, at an estimated rate of 2.2% per annum, such that many urban and peri-urban animals no longer experience natural darkness. The majority of animal species have evolved under bright days and comparatively dark nights, with their physiology and behaviour synchronised to this rhythm. Accordingly, disruption to this cycle is linked to a suite of behavioural and physiological shifts across taxa. Experimental and correlational evidence documenting phenotypic responses to the presence of artificial light at night are accumulating but the underlying mechanisms driving the observed negative impacts associated with artificial light at night are not resolved. A likely reason is that light at night disrupts circadian rhythms and contributes to perturbed oxidative status through its interaction with the indolamine, melatonin, a key driver of circadian rhythm and powerful antioxidant. A major and currently untested gap in the literature is whether light at night can act as a driver of evolutionary change. In this thesis, I investigated the short-term phenotypic impacts of ecologically relevant levels of artificial light at night on life history traits (throughout Chapters 2 to 5) and oxidative status (Chapters 2 and 4), using the model organism Drosophila melanogaster. I then used experimental evolution to explore whether artificial light at night can induce local adaptation in populations evolved over 15 to 25 generations (Chapter 4). Finally, using a melatonin dietary supplementation experiment, I attempted to investigate the relationship between artificial light at night and the melatonin pathway, thus hoping to demonstrate disruption to the melatonin pathway as a causal mechanism underpinning the observed phenotypic responses (Chapter 5). My results demonstrated experimentally, that individuals exposed to artificial light at night have short-term phenotypic changes, with disrupted mating behaviour, reduced fecundity and size, altered development patterns and reduced longevity in D. melanogaster (Chapters 2 to 5). Additionally, I present novel (and somewhat counter intuitive) evidence, that artificial light at night is associated with lower levels of reactive oxygen species in ovaries (Chapter 3) and, aligned with this, reduced oxidative DNA damage in female flies (Chapter 4). In contrast, I found no evidence for such effects in males (Chapters 3 and 4). Despite potential for evolutionary change, I found little evidence for adaptation in most fitness traits after evolution under artificial light at night (Chapter 4), with mating propensity the only life history trait to exhibit limited local adaptation. This suggests that the selective pressure of artificial light at night in the laboratory, may be weaker than anticipated. However, the fact that some level of adaptation was evidenced in relatively benign conditions, suggests that, in a more natural competitive environment, the selection pressure of light at night may be stronger. I was unable to conclude whether melatonin is a potential mechanism driving phenotypic variation following exposure to light at night (Chapter 5), as the melatonin doses and design used, despite replicating a previous study, resulted in negative fitness consequences (reduced longevity under dark nights and disrupted eclosion regardless of light treatment), suggesting the melatonin supplementation was potentially toxic. Nonetheless, these data potentially support the importance of circadian disruption under artificial light at night as a driver of the observed negative effects. I propose that further research is warranted to test different melatonin concentrations and dosage duration at different life stages and at different times relative to circadian rhythm. This variation in dosage regimens may be able to better define its role (and the relevant contributions of circadian disruption and oxidative status) in the effects of artificial light at night. This thesis demonstrates the negative impacts of artificial light at night in the model species, D. melanogaster and adds to the growing body of literature documenting taxa-wide damaging effects of artificial light at night on animal behaviour and physiology. As we continue to light our nights and reduce natural darkness globally, understanding the consequences and mechanisms behind the effects of artificial light at night is paramount to informed decision making around urban lighting strategies. Moreover, understanding the role of artificial light at night in driving evolutionary change, is of the utmost importance in maintaining wildlife stability in an increasingly urbanised world.
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ItemThe physiological effects of artificial light at night on the Australian black field cricket( 2018)The presence of artificial light at night (ALAN) is one of the fastest growing, most pervasive and, until recently, under-appreciated forms of global pollution. Current ALAN levels in urban environments are associated with changes to animal behaviour, dramatic shifts in the timing of life history events, reductions in individual fitness and disrupted physiological processes, including immune function. This thesis explores the physiological effects of ecologically relevant levels of ALAN on a model invertebrate species, the Australian black field cricket, Teleogryllus commodus. In Chapter 1, I reviewed the literature with a particular emphasis on the physiological effects of ALAN, including growth, survival, reproductive success, and immune function. I also speculate as to the potential mechanistic links behind these ALAN induced biological effects. In Chapter 2, I explored experimentally the effects of ecologically relevant levels of ALAN (1, 10 and 100 lux) on life history and fitness traits of the black field cricket. Under controlled laboratory conditions, I reared crickets from egg to adult in an environment with either no ALAN (0 lux) or one of the above dim-ALAN intensities and assessed the consequences of ALAN for growth, survival and reproductive success. I demonstrated that egg hatch, adult survival and reproductive measures were largely unaffected by the presence of ALAN, however juvenile development time was longer and adults were larger when crickets were exposed to any light at night (1, 10 or 100 lux). In Chapter 3, I examined the effects of ALAN (1, 10 and 100 lux) on three key measures of adult immune function (haemocyte concentration, lytic activity, and phenoloxidase activity). The presence of any ALAN (1, 10 or 100 lux) had a clear negative effect on the cellular immune response. Specifically, individuals exposed to any ALAN were unable to increase their haemocyte concentration in response to a stressor challenge. In Chapter 4, I investigated a novel method for the measurement of circulating melatonin in small samples of cricket haemolymph using high-performance liquid chromatography tandem mass spectrometry, with methyl tert-butyl ether (MTBE)/ethyl acetate as an extraction agent. The calibration curve for melatonin was linear in the range of 0.25 and 10 pM (R2 = 0.999), and the limit of detection was 0.25pM. When applied to a set of pilot data from crickets reared under different ALAN environments (0, 1, 10, and 100 lux), the results were however inconclusive, due to small sample sizes. In Chapter 5, I discuss the significance of these findings and their ecological implications. My thesis advances our understanding of the biological ef fects of ALAN for invertebrates, a key taxon contributing to ecological community structure and composition. It is one of the first set of studies to simultaneously investigate multiple traits in the same individuals exposed to lifelong ALAN, and to assess changes in immune function throughout their adult life. Combined, the results presented demonstrate a disruption to physiological processes, and highlight the potential for ALAN to alter the phenology of communities and reduce the overall fitness of individuals.