Investigating the mechanisms behind asymmetric cell division (ACD) not only provides insight into an integral aspect of development in organisms such as C. elegans, D. melanogaster, and in human stem cells, but it also has the potential to elucidate the cellular functions that result in disease processes like cancer. ACD describes the cellular activity that results in a singular parent cell dividing into two daughter cells with two distinctive molecular compositions, and, in turn, fates. Drosophila melanogaster neural stem cells, called neuroblasts, are intrinsically polarized and divide asymmetrically. This process involves an uneven distribution of cell-fate-determining proteins that eventually designate the function of the daughter cell. Because of this polarity establishment and orientation, these daughter cells can have highly specialized functions. My work uses Drosophila melanogaster neuroblasts to screen for novel mutations responsible for compromising ACD. I'm specifically interested in finding genes that are involved in the generation of cell size asymmetry. Finding these mutations is imperative because, by doing so, we can identify critical genes involved in this process of interest. To that end, I knocked-down candidate genes with RNAi in neuroblasts and assayed the localization dynamics of myosin and microtubules– two critical components of the ACD and symmetric division process. Through confocal, live-cell imaging, I then examined the dynamics of these cellular proteins as they relate to wild-type ACD to see if my chosen candidates were responsible for this process. I anticipate finding novel cytoskeleton regulators that are important for establishing cell size asymmetry. In the future, finding the genes behind ACD will provide great insights into the mechanisms behind both development and disease in addition to the field of stem cell biology overall.

Recently there has been interest in two possible sources of mass in the outer solar system. First, observations of recently discovered remote outer solar system objects have suggested the presence of a ninth planet. Different numerical simulations have suggested either a less massive (1.5-3 Earth masses) planet with a semimajor axis of 250-500 AU from the Sun (the Earth orbits at 1 AU), or a more massive (5-15 Earth masses) planet at 400-800 AU. Second, data from the New Horizons spacecraft has suggested that there may be an additional roughly circular belt of objects, similar to the Kuiper Belt, beyond 60 AU. This raises the question of whether this belt would be compatible with some or all of the proposed forms of planet 9. To answer this question, I ran a series of orbital dynamics simulations with randomly generated test particles representing the proposed second Kuiper Belt, and different masses and orbital parameters for planet 9. By looking at how planet 9 changed the orbits of the test particles over the period of the simulation, I concluded that although planet 9 would not significantly affect objects orbiting at 60-100 AU, in the most extreme cases, it would significantly broaden the distribution of orbital inclinations of objects beyond 100 AU. Astronomical deep and wide surveys conducted over the next few years have the potential to detect both planet 9, and objects beyond the Kuiper Belt. If second Kuiper Belt objects are discovered, these objects having a wider-than-expected range or orbital inclinations would point to gravitational disturbances, such as those caused by planet 9. Alternatively, if planet 9 is discovered, these simulations suggest that a second Kuiper Belt would need to be more inclined than has been so far assumed.

The effects of the fungal pathogen Swiss needle cast (SNC) on its host species, Douglas-fir, and its timber harvest repercussions have been researched. However, more research is needed regarding the effects of SNC on understory species and, consequently, browsing ungulate species. This study analyzes the effects of various thinning methods on SNC and SNC’s influence on understory species richness, diversity, and cover. The goal is to articulate a clear dynamic of SNC in Sitka spruce and Douglas-fir - western hemlock zones to provide insights for guiding forest management. I will analyze the Olympic Natural Resource Center’s pre and post-treatment data from Siuslaw National Forest with statistical analyses to articulate patterns in SNC presence, thinning, and understory change. The early, mid, and late seral/thinned treatments vary in density and by species replanted. I expect that thinning will decrease SNC abundance and increase understory species richness. Additionally, I predict that the stands replanted with red alder and conifers will see a higher abundance of understory due to red alder’s nitrogen-fixing ability. The enhanced understanding of SNC and thinning’s interplay aims to educate current and future forest managers about ecologically responsible management.

Down syndrome (DS, trisomy 21) is the most common chromosomal condition, affecting 1 in 700 live births. In addition to neurodevelopmental issues, people with DS also have an increased susceptibility to infections such as influenza and COVID. Altered immune function is one likely driver. Additionally, non-immune factors may also contribute. For example, upregulation of TMPRSS2, an enzyme that promotes cellular entry of SARS-COV2 encoded on chromosome 21, may predispose people with DS to severe SARS-CoV2 infection. This project builds on recent data from the Khor lab that suggests a link between DS and susceptibility to malarial infection. P. vivax is a parasite that causes malaria and is endemic across wide regions, from South America to South Asia. P. vivax enters cells through a protein called Duffy which is a chemokine receptor on the surface of red blood cells (RBCs). Recent profiling of whole blood from patients with DS showed dysregulation of many genes. Geneset enrichment analyses identified heme metabolism as the second most affected pathway. Within these heme metabolism genes, ACKR1, the gene encoding Duffy, was particularly and disproportionately upregulated. This suggests that people with DS may express higher levels of the Duffy protein on their RBCs, which in turn may predispose to P. vivax infection. This project seeks to better understand and validate how Duffy expression is dysregulated in people with DS. The goal of the project is to quantify the level of Duffy present in the RBC’s of patients with and without DS. If validated, the next step will be to test the susceptibility of these cells to malaria. This may point to a need for altered clinical management of malaria in people with DS and inform further studies looking at the mechanistic differences in RBC biology in people with DS.