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I am evaluating the genomic basis of a model of heat tolerance in which organisms succumb to warming when their demand for oxygen exceeds their supply. This model predicts that tolerance of hypoxia should correlate genetically with tolerance of heat. To evaluate this prediction, I tested heat and hypoxia tolerance

I am evaluating the genomic basis of a model of heat tolerance in which organisms succumb to warming when their demand for oxygen exceeds their supply. This model predicts that tolerance of hypoxia should correlate genetically with tolerance of heat. To evaluate this prediction, I tested heat and hypoxia tolerance in several genetic lines of Drosophila melanogaster. I hypothesized that genotypes that can fly better at high temperatures are also able to fly well at hypoxia. Genotypes from the Drosophila Genetic Reference Panel (DGRP) were assessed for flight at hypoxia and normal temperature (12% O2 and 25°C) as well as normoxia and high temperature (21% O2 and 39°C). After testing 66 lines from the DGRP, the oxygen- and capacity-limited thermal tolerance theory is supported; hypoxia-resistant lines are more likely to be heat-resistant. This supports previous research, which suggested an interaction between the tolerance of the two environmental variables. I used this data to perform a genome-wide association study to find specific single-nucleotide polymorphisms associated with heat tolerance and hypoxia tolerance but found no specific genomic markers. Understanding factors that limit an organism’s stress tolerance as well as the regions of the genome that dictate this phenotype should enable us to predict how organisms may respond to the growing threat of climate change.
ContributorsFredette-Roman, Jacob Daniel (Author) / Angilletta, Michael (Thesis director) / VandenBrooks, John (Committee member) / Youngblood, Jacob (Committee member) / School of Life Sciences (Contributor, Contributor) / Barrett, The Honors College (Contributor)
Created2020-05
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The non-native mosquito Aedes aegypti has become a common nuisance in Maricopa county. Associated with human settlement, Ae. aegypti is known to reproduce in standing water sources both indoors and outdoors, within vessels such as tires, flowerpots, and neglected swimming pools (Jansen & Beebe, 2010). Ae. aegypti and the related

The non-native mosquito Aedes aegypti has become a common nuisance in Maricopa county. Associated with human settlement, Ae. aegypti is known to reproduce in standing water sources both indoors and outdoors, within vessels such as tires, flowerpots, and neglected swimming pools (Jansen & Beebe, 2010). Ae. aegypti and the related Ae. albopictus are the primary vectors of the arboviral diseases chikungunya, Zika, yellow fever and dengue. Ae. aegypti tends to blood feed multiple times per gonotrophic cycle (cycle of feeding and egg laying) which, alongside a preference for human blood and close association with human habitation, contributes to an increased risk of Ae. aegypti borne virus transmission (Scott & Takken, 2012). Between 2010-2017, 153 travel-associated cases of dengue were reported in the whole of Arizona (Rivera et al., 2020); while there have been no documented locally transmitted cases of Aedes borne diseases in Maricopa county, there are no apparent reasons why local transmission can’t occur in the future via local Aedes aegypti mosquitoes infected after feeding from travelling viremic hosts. Incidents of local dengue transmission in New York (Rivera et al., 2020) and Barcelona (European Center for Disease Control [ECDC], 2019) suggest that outbreaks of Aedes borne arbovirus’ can occur in regions more temperate than the current endemic range of Aedes borne diseases. Further, while the fact that Ae. aegypti eggs have a high mortality rate when exposed to cold temperatures limits the ability for Ae aegypti to establish stable breeding populations in temperate climates (Thomas, Obermayr, Fischer, Kreyling, & Beierkuhnlein, 2012), global increases in temperature will expand the possible ranges of Ae aegypti and Aedes borne diseases.
ContributorsHon, Ruiheng (Author) / Paaijmans, Krijn (Thesis director) / Bond, Angela (Committee member) / Angilletta, Michael (Committee member) / School of Molecular Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2020-05
Description
****Project Disclaimer: Unfortunately due to the COVID-19 outbreak during Spring 2020, ASU shut down in-person classes and campus facilities as means to prevent the spread of the virus. This meant though that a polished final podcast recording was unable to be made. Instead, a first-run, practice podcast recording that was

****Project Disclaimer: Unfortunately due to the COVID-19 outbreak during Spring 2020, ASU shut down in-person classes and campus facilities as means to prevent the spread of the virus. This meant though that a polished final podcast recording was unable to be made. Instead, a first-run, practice podcast recording that was recorded before the shut down is uploaded in its stead as a reference as to how the final was intended to sound and be produced. ****


Cellular hypertrophy is an anaerobically-based, adaptive process that mammalian skeletal muscle undergoes in response to damage resulting from unaccustomed force generation by the muscle. Hypertrophy allows for the muscle tissue to recover from the immediate injury and also to be rebuilt more capable of withstanding producing the same amount of force without injury, should it happen again. This means the end result of an adapted muscle is an overall more efficient tissue. The ability to regenerate after damage to the structure and function of the muscle tissue is a highly orchestrated event involving multiple steps and key events to occur. Most briefly, a mechanical load is attempted to be lifted but due to demanding a high amount of contractile force to lift, it causes microdamage to the structural and contractile elements of muscle fiber’s sarcomeres. In addition to an inflammatory response, satellite cells, as a part of a myogenic response, are activated to invade the fiber and then permanently reside inside to produce new proteins that will replace the damaged and necrotized proteins. This addition of cellular content, repeated over multiple times, results in the increased diameter of the fibers and manifests in the visual appearance of skeletal muscle hypertrophy. These steps have been listed off devoid of the contexts in which it takes for these to occur and will be addressed within this thesis.
ContributorsDwyer, Lauren Mingna Carol (Author) / Hyatt, JP (Thesis director) / Kingsbury, Jeffery (Committee member) / School of Life Sciences (Contributor) / School of Art (Contributor) / Barrett, The Honors College (Contributor)
Created2020-05