2020 Abstracts

Davis, Morgan; Edvalson, Logan; Busath, David (Brigham Young University)
Faculty Advisor: Busath, David (Life Science, Physiology and Developmental Biology)

Influenza infection, and subsequent pneumonias, are the cause of over fifty thousand deaths in the United States per year, and, according to the CDC, influenza is the 8th leading cause of death in this country. Research into the pathogenesis of influenza elucidates critical interactions that take place during different phases of infection which can be targeted by novel drug therapies. Our lab has focused on discovering the role of of PDGFR and VEGFR and other Receptor Tyrosine Kinases (RTKs) in aiding viral infection. RTK activation is reported to be important for successful viral infection, and our project has focused on three different RTKs: VEGFR, PDGFR, and endothelial growth factor receptor (EGFR). In these experiments, Madin Darby Canine Kidney (MDCK) cells were bathed in growth medium containing a specific RTK inhibitor, and then infected with the influenza virus. The vitality of the cells was measured using crystal violet staining and spectrophotometer results. The data showed that using a drug called imatinib—a potent PDGFR inhibitor—resulted in the highest cellular vitality while VEGFR inhibitors developed here at BYU also showed anti-influenza activity. This suggests that the influenza virus is at least partially dependent on PDGFR and VEGFR activation to enhance its life cycle. Future experimentation will study which of the many branches of these receptor's phosphorylation cascades are being utilized by the virus.

Edwards, Taylor; Ram, Akila; McCarty, Ashley; Bobeck, Erin N (Utah State University)
Faculty Advisor: Bobeck, Erin (College of Science, Biology Department)

First-line chemotherapies against solid tumors are highly efficacious in reducing the tumor burden, but have many adverse side-effects including nerve damage, leading to chronic pain. Non-addictive, efficacious pain relievers are an area of active interest, and we propose a novel target to address this pressing issue. GPR171 is a G-Protein Coupled Receptor that was recently deorphanized and was identified to be expressed in the brain in regions that regulate reward, anxiety, and pain. Within the pain circuit, it was shown previously that systemic administration of the GPR171 agonist enhances morphine antinociception in acute pain tests. Preliminary data from our lab has shown that GPR171 activation can also alleviate persistent inflammatory pain. However, the role of this receptor has not been investigated in other chronic pain models. Given these findings in acute and inflammatory pain, we hypothesize that GPR171 can reduce neuropathic pain. To test this hypothesis, we investigate the role of GPR171 in chronic neuropathic pain. We tested the efficacy of a GPR171 agonist in a chemotherapy-induced neuropathy mouse model. Neuropathic pain was induced by injecting paclitaxel (16 mg/kg) followed by assessment of the pain-relieving effects of activating GPR171 receptors. Mechanical pain thresholds were assessed using Von Frey filaments. We observed an increase in mechanical thresholds following GPR171 agonist treatment. Further, using immunofluorescence we observed that there is a decrease in GPR171 receptors in the periaqueductal gray (PAG) of these mice that have neuropathic pain, indicating that the agonist can bind to the available receptors to produce pain relief. Overall, this study proposes that GPR171 may be a novel target for the treatment of neuropathic pain.

Bonnett, Kelsie; Golden, Kaitlyn; Johnson, Jerry (Brigham Young University)
Faculty Advisor: Johnson, Jerald (Brigham Young University, Biology)

Understanding life-history strategies allows us to know how a changing environment affects species and communities. Livebearing Poeciliid fish are commonly used as models to gain a better understanding of these strategies, but some species like Alfaro cultratus have been neglected in this process. A. cultratus is a freshwater fish with a unique keel-shaped anal fin commonly found along the eastern coast of Central America. To understand the life-history strategies of this species and use it as a future model, I am performing an experiment to: 1) determine if there is sexual selection in Alfaro cultratus considering both body size and anal fin length; 2) determine whether A. cultratus displays sexual selection; and 3) understand how predation influences both dimorphism and selection. To do this I will be performing a two-part experiment in which I will first analyze previously collected samples for morphological differences, and second perform a live experiment to test Alfaro female preference. By doing so I will be able to not only advance our understanding of A. cultratus, but of life-history theory and conservation strategies.

Szulik, Marta; Wang, Li; Franklin, Sarah. (University of Utah)
Faculty Advisor: Franklin, Sarah (Medicine, Internal Medicine)

Heart failure (HF) is a type of heart disease characterized by the structural and functional impairment of ventricular filling. In 2016, HF was the underlying cause of death in approximately 78,000 individuals and today more than 6.2 million Americans suffer from heart failure. HF is the final stage for many types of heart disease including cardiac hypertrophy. During hypertrophy, the ventricular walls thicken to help maintain the proper workload needed to continue supplying the body with oxygenated blood. In addition to increase in cell size, cardiac hypertrophy leads to cell death, fibrosis, metabolic reprogramming and reactivation of fetal gene expression. Gene expression is often modulated by changes in chromatin and histone structure via post-translational modifications (PTMs). Histone methylation, a covalent PTM, has been shown to play a significant role in cardiac development.

Smyd1 is a muscle specific lysine histone methyltransferase protein that has a role in early cardiac development and is known to methylate histone H3 on lysine-4. Additionally, loss of Smyd1 in adult mice models has been shown to induce heart failure and hypertrophy whereas overexpression of Smyd1 has been shown to restrict hypertrophic growth in cell model. Although Smyd1 knockdown experiments have been performed in vivo, the effects of knocking down Smyd1 in isolated cardiomyocytes has not been examined. Furthermore, the effects Smyd1 overexpression in adult mammalian heart failure is unknown.

This project seeks to characterize changes in global levels of histone PTM's as a result of either overexpressing or silencing Smyd1. Using proteomic analysis, we have identified the changes in histone methylation and consequently gene expression in the adult heart and isolated cells in response to Smyd1. Our results help us better understand Smyd1 role in the failing heart and help determine it therapeutic potential.

Smith, Chyanne; Jal, Tumursukh; Duuji, Nyam-Ochir; Tumur, Battogtokh; Mull, John (Weber State University)
Faculty Advisor: Mull, John (Weber State University, College of Science; Zoology)

The Darhad Valley, Mongolia, is a sparsely populated area with abundant wildlife and numerous livestock, including: goats, yaks, horses, and sheep. Few studies completed in this location have placed an importance on obtaining baseline species data. To our knowledge, no data have been collected on small mammal diversity, density, and distribution. This study focused on live-trapping small mammals, with an emphasis on rodents, in six locations throughout the Darhad. We aimed to identify species currently present and develop protocols for future work. Captured rodents represented four families: Sciuridae, Arvicolinae, Cricetidae, and Muridae. Common species included striped dwarf hamsters (Cricetulus barabensis), Mongolian silver voles (Alticola semicanus), and Korean field mice (Apodemus peninsulae). Challenges encountered, which must be mitigated in future studies, include: curious humans, resource and waste management, grazing animals, and novel food sources. These studies should also emphasize community composition, range, and presence of ectoparasites, which could transfer zoonotic diseases.

Frandsen, Paul; Bursell, Madeline; Taylor, Adam; Wilson, Seth; Steeneck, Amy; Stewart, Russell (Brigham Young University)
Faculty Advisor: Frandsen, Paul (Life Sciences, Plant and Wildlife Sciences)

Caddisfly (Insecta: Trichoptera) silk is unique from other insect's silk in that it retains its adhesive capabilities, strength and viscoelasticity when submerged in water. To understand how caddisfly silk is capable of possessing these characteristics, it is essential to understand the protein foundation of the silk proteins. Caddisfly silk is complex and made up of different structures generated by processes that are unique to caddisfly silk. H-Fibroin and L-Fibroin have been identified as two of the major protein components within caddisfly silk (Hatano & Nagashima, 2015). The caddisfly silk fibre experiences unique structures not typically seen in nature. An understanding of the primary structure of the silk fibre is essential in understanding the complexity of the silk's capabilities. In this study, we used proteomic techniques to analyze the complex H-Fibroin protein and the silk fibre in order to look at the underlying structural features of the protein. In doing so, we identified post-translational phosphorylation, metal cation incorporation, and other structural features which contributes to Caddisfly silk's adhesive capabilities, strength and viscoelasticity when submerged in water.

Boyce, Zach; Smith, Calvin; Martin, Ashlyn; Ketch, Yuko; Dugan, James; Wright, Cole (Brigham Young University)
Faculty Advisor: Jeffrey, Edwards (Brigham Young University, Physiology and Developmental Biology)

Post-traumatic stress disorder (PTSD) is a complex psychological disorder that affects about 1 of 4 individuals after a stressful/traumatic experience. One common model to induce PTSD in rats is social defeat (SD) combined with chronic light exposure. First, we screened rats for natural anxiety to use in the SD protocol. Next, elevated plus maze (EPM) and light-dark transition (LDT) tests were used to detect anxious behavior after SD. The SD protocol induced significant anxious behavior when compared to controls. Next, we performed long-term potentiation (LTP) field electrophysiology synaptic plasticity physiology experiments in brain slices of the ventral hippocampus (VH) and basolateral amygdala (BLA), regions known to have altered enhanced plasticity in PTSD. SD significantly increased LTP in the VH (~25% greater than control) and BLA (~35% greater than control). To determine whether a prophylactic treatment could prevent the physiological changes of PTSD, we simultaneously administered two drugs at 10 mg/kg doses by intraperitoneal injection one week prior to and for the duration of SD. The first, propranolol, is a beta-adrenergic receptor antagonist, and the second, mifepristone, is a glucocorticoid receptor antagonist; thus, treatment would target the action of stress hormones altered in PTSD. To determine whether a prophylactic treatment could prevent the physiological changes of PTSD, propranolol and mifepristone, antagonists of two stress receptors, were simultaneously administered at 10 mg/kg doses by intraperitoneal (IP) injection one week prior to and for the duration of SThese drugs significantly decreased LTP in the VH and BLA back to near-control levels while SD rats with vehicle injections still had elevated LTP. However, SD drug-treated rats did not show significant reductions in anxious behavior compared to non-injected SD rats and also exhibited significantly more anxious behavior than control rats, suggesting the IP injection induced added stress. Next, we used rtPCR to examine gene expression of drug targets and plasticity markers to determine potential mechanisms for observed LTP changes. In both the VH and BLA, SD was associated with a significant decrease in glucocorticoid and mineralocorticoid receptor expression, which was restored to control levels under drug treatment. Overall, our data suggest that propranolol and mifepristone together may be a potential prophylactic treatment for preventing PTSD through a mechanism likely mediated by glucocorticoid/mineralocorticoid receptors.

Hales, Emily; Lundgren, Jane; Carter, John; Kempton, Colton; Johnson, Steven (Brigham Young University)
Faculty Advisor: Johnson, Steven (Brigham Young University, Molecular and Microbiology)

The mechanisms of transgene silencing in C. elegans are poorly understood, despite the importance of the nematode as a model for genetic research. Insertion of a transgene led to the expression of GFP in both the body wall and pharyngeal muscle cells of C. elegans as expected. However, subsequent generations stopped expressing body wall GFP. To reverse silencing, we have flanked the enhancers responsible for GFP expression with 601 sequences. The 601 sequence strongly positions nucleosomes. We hypothesize that this positioning will eliminate transgenerational gene silencing of body wall GFP.

Ashley McCarty, Akila Ram, Max V. McDermott, Erin N. Bobeck (Utah State University)
Faculty Advisor: Bobeck, Erin (College of Science, Biology Department)

Morphine is a potent opioid analgesic, but its long term use can lead to negative side effects, including tolerance, which is a decrease in the effectiveness of the opioid. An area of active interest is looking into the molecular effects of chronic morphine treatment in the Periaqueductal gray (PAG), a brain region that controls descending pain modulation. One such molecular target within the PAG is extracellular-signal regulated kinase 1/2 (ERK). Previous studies have shown that pharmacological inhibition of ERK enhanced morphine tolerance, indicating that ERK activity is associated with better responsiveness to morphine. The PAG is known to contain a heterogenous population of neurons including GABA and glutamate subtypes. However, which neurons ERK is activated in within the PAG following morphine tolerance is unknown. Further, there are known differences in PAG activity between male and female mice. However, these sex-differences have not been well studied after morphine tolerance using acute pain tests. The purpose of this research is to investigate differences in ERK activation following morphine tolerance in male and female mice. We treated wild-type male and female mice with morphine (10 mg/kg, i.p.) or saline for 5 days to induce morphine tolerance, following which both behavior and protein immunofluorescence were assessed. We observe sex-specific differences in ERK activation levels and morphine antinociceptive tolerance in mice. We also assessed co-localization of ERK with GABA and glutamate neurons after morphine tolerance. The study will help us understand the cell-type specificity of kinase activation following morphine tolerance. Further this will give us more information about the nature of neurons that are contributing to sex-differences in opioid functions within the PAG

Jensen, Daelin; Baxter, Melanie (Brigham Young University)
Faculty Advisor: Tessem, Jeffery (Nutrition, Dietetics, and Food Science; Life Sciences)

Approximately 1.25 million people are currently living with type 1 diabetes. By 2050, 5 million people are expected to be diagnosed with the disease1. The insulin secreting pancreatic beta cells are essential to control proper glucose absorption and storage in insulin sensitive peripheral tissue. Both type 1 and type 2 diabetes are characterized by decreased functional beta cell mass and, consequently, decreased insulin production. One potential intervention is the use of beta cell transplantation from cadaveric donors. A major impediment to greater application of this treatment is the scarcity of transplant ready beta cells. Increasing the quantity of functional beta cells for transplantation will lead to increased insulin production and better management of the disease. Various genes have been defined that can induce beta cell replication. A major caveat of these findings, however, is that these factors induce replication in young beta cells but not in aged beta cells. Age-dependent morphological changes in the beta cell are poorly understood, despite its relevance to type 1 diabetes: here, we show that insulin-positive tissue area changes with age. Given that the majority of beta cells that will be used for transplant will come from aged donors, it is imperative to understand why aged beta cells are refractory to the aforementioned proliferative mechanisms. The cell cycle is tightly regulated by cyclin-dependent kinases. Cyclin-dependent kinase inhibitors (CDKI's) bind to cyclin dependent kinases, inhibiting cell proliferation. We hypothesized that these CDKIs are responsible for the observed lack of proliferation in aged animals. We demonstrate the expression of the Ink4 and Cip/Kip family of CDKI's by mRNA, protein and histological expression in 5 week and 5 month old primary rat beta cells. In addition, we show how size-related expression differences of CDKIs relate to beta cell proliferation.

Hannah A. Veltkamp, Sydney Houghton, Michael T. Stevens (Utah Valley University)
Faculty Advisor: Stevens, Micheal (Utah Valley University, Biology)

Netleaf hackberry (Celtis reticulata) is a deciduous shrub native to the southwestern United States and northern Mexico. Individual shrubs can be long-lived, but newly established stands of hackberry are rare. The lack of juvenile hackberry in the wild could be due to low germination rates reported in both laboratory and field settings. The seeds of hackberry are embedded in drupes that are an important source of food for birds and small mammals. Animals likely play an important role in seed dispersal, and passing through a digestive tract could increase the germination rates of hackberry seeds. Passage through the digestive tract of a mammal can increase the germination rates for some plant species, but not for others. We hypothesized that passage through the digestive tract of a coyote would increase the germination rates of C. reticulata. To test this hypothesis, we collected 17 coyote scats containing visible hackberry fruits from along the Bonneville Shoreline Trail east of Provo, Utah, using latex gloves. Each scat location was recorded using a GPS unit. After collecting each scat, we found the closest hackberry shrub and picked a sample of fresh hackberry fruits from it. All samples were cleaned and cold stratified and then planted into cone-tainers containing a potting soil mix and placed in the Utah Valley University greenhouse. We sowed 20 seeds from each of the 17 coyote scats and

20 seeds from each of the neighboring hackberry bushes for a total of 680 seeds. The 680 cone-tainers were labeled with plastic stakes and randomly positioned into trays that were randomly distributed on a bench in the greenhouse. The seeds, and later seedlings, were watered as needed (typically three days/week). On watering days, we checked for newly-germinated hackberry seedlings and recorded their date of emergence. Near the end of the experiment, we measured the height of each seedling. The germination rate of hackberry seeds that had passed through the

digestive tract of a coyote did not differ from the germination rate of seeds from fresh-picked fruit (42.7% vs. 46.5%, respectively; _ 2 = 0.558, df = 1, p = 0.455). However, on average, the coyote-treatment seeds took just over half as many days to germinate as did the seeds from fresh-picked (undigested) fruit (35 days vs. 69 days, respectively; p < 0.001). The seedlings from coyote-treatment seeds were 9.5% taller than were the seedlings derived from seeds from undigested fruit (6.4 cm vs. 5.8 cm, respectively; p < 0.001). Our results show that consumption by coyotes can benefit hackberries by enabling their seeds to germinate earlier in the year when

conditions for establishment are good. The earlier start on germination that coyote-ingested hackberries get translates to increased height and likely a higher rate of survival in the field.

Elison, Weston; Bauchle, Casey; Bunker, Libby; Stephens, Samuel; Tessem, Jeffery (Brigham Young University)
Faculty Advisor: Tessem, Jeffery (Brigham Young University; Nutrition, Dietetics and Food Science)

Type 2 Diabetes (T2D) effects hundreds of millions of people worldwide, with that number increasing rapidly. It is characterized by increased insulin resistance and dysfunctional insulin secretion. The beta cell of the pancreas is the primary insulin secreting tissue, found in the endocrine tissue of the pancreas called islets of Langerhans. In T2D beta cells become glucose intolerant and disease progression is characterized by loss of functional beta cell mass. Previous studies have shown that the transcription factor Nkx6.1 is vital for beta cell differentiation, identity, and insulin secretion. Research has indicated that Nkx6.1 expression and protein levels decrease in pancreatic islets from human donors with T2D. Our data indicates that glucolipotoxicity, a common model for obesity and diabetes in cell culture, leads to decreased Nkx6.1 mRNA expression, protein levels and nuclear localization in Ins-1 832/13 cells. Nkx6.1 regulates genes in the nucleus , and its loss inhibits proper insulin secretion. We propose that reactive oxygen species created by metabolism of excess fuel decreases Nkx6.1 expression and Nkx6.1 target gene expression, as measured by quantitative polymerase chain reaction (qPCR). Also, increased glucose concentrations causes increased Nkx6.1 protein degradation and translocation out of the nucleus. Protein levels will be measured by western blot and localization by confocal microscopy. In order to understand how these changes effect beta cell function, we will measure glucose stimulated insulin secretion by sandwich Enzyme Linked Immunosorbent Assay (ELISA). We further propose that Nkx6.1 overexpression will restore beta cell function. These results will assist in unraveling the cause of beta cell dysfunction in T2D.

Karin, Kettenring; Robison, Talin; Leonard, Emily (Utah State University)
Faculty Advisor: Kettering, Karin (S.J. & Jessie E. Quinney College of Natural Resource, Watershed Sciences Department)

The Great Salt Lake (GSL) and its wetlands are important habitat for migrating birds. The GSL wetlands provide crucial habitat for nesting, food, and areas to recover from migration. Common carp are a threat to GSL wetlands. Carp disturb sediments in the water, blocking some of the sunlight from entering the water, which is utilized by aquatic macrophytes and algae. Carp also may be affecting invertebrate populations, which are critical food resources for migrating birds, but these effects have not been well-documented. My research addressed the question: what are the effects of invasive common carp on invertebrate food sources for diving ducks in the Great Salt Lake wetlands? I answered my research question by addressing the following objectives: (1) to identify the benthic, epiphytic, and water-column dwelling invertebrates in Farmington Bay Waterfowl Management Area (WMA), and (2) to determine if common carp are having an impact on the overall density, diversity, and abundance of the invertebrate communities fed on by diving ducks. I compared invertebrate communities (diversity and abundance) between carp-excluded boxes and control boxes. I constructed my carp exclosures of wire mesh and t-posts to prohibit carp from entering while still allowing invertebrates and water to freely move in and out of the exclosure. The control boxes were constructed of t-posts and allowed carp to freely enter and exit the box. I used dipnet and substrate core samples to determine what invertebrates are living in the water column and substrates at Farmington Bay wetlands. Although sample processing is on-going, early results indicate that carp reduce water column invertebrate abundance while effects on invertebrate diversity are thus far inconclusive. Given the importance of GSL wetlands and their invertebrate food sources to migrating diving, my research findings underscore the importance of aggressive carp management.

Gottfredson, Sarah; Chaston, John (Brigham Young University)
Faculty Advisor: Chaston, John (Life Sciences, Plant and Wildlife Sciences)

The microbiome of Drosophila melanogaster can have significant effects on the host, and many of these have been studied. However, the reason why the bacterial species associate with and persist in D. melanogaster has not been studied in depth. Here we define persistence as how long a microbe associates with a host. The early assumption has been that the D. melanogaster gut microbiome is established solely through diet, but recent work suggests that other factors may be at play in the microbiome establishment. This experiment aims to study the correlation between bacterial genotype and persistence in the D. melanogaster microbiome. In this study, a metagenome wide association (MGWAS) was done using 40 different strains of bacteria to find distinct bacterial genes that are significantly correlated with persistence. To do this, each strain was mono-associated with twenty-four individual flies. The flies were reared for fourteen days, transferred onto new food three times a day for two days, homogenized, and plated. Using the significant genes found through the MGWAS, the same experiment protocol will be used to test mutants of these genes for their effect on persistence. These data will provide us with distinct genes that are necessary for effective bacterial persistence.

Evans, Justin; Murray, Cameron; Crowley, Bailey; Welker, Dennis; (Utah State University)
Faculty Advisor: Welker, Dennis (College of Science, Biology Department)

In previous experiments, we explored the abilities of a set of newly derived vectors to transform Lactobacillus casei, specifically, the 32G and the A2-362 strains. We have now expanded our research to study the abilities of these vectors to transform additional Lactobacillus species, Lactobacillus paracasei strain LPC-37 and Lactobacillus rhamnosus strain HN001. The vectors were transformed into the cells by electroporation, after which the cells were given a 4-hour incubation to allow expression of the erythromycin resistance gene carried on the vectors. The cells were then plated to MRS agar containing erythromycin and incubated for 2-3 days until colonies appeared. The colonies were counted and the transformation efficiencies for each vector tabulated as colony forming units per _g of vector DNA. These studies help us to understand how effective the vectors are at transforming different species of lactic acid bacteria. We can also start to ask why some vectors performed better in some bacterial strains than they did in other strains.

Not yet published (Brigham Young University)
Faculty Advisor: Chaston, John (Brigham young University, Life Sciences)

Within an organism's gut are many strains of bacteria that are constantly interacting with their host. Microbiota composition has been shown to impact many aspects of host health such as metabolism, fat-storage, starvation resistance, and reproduction. Certain behaviors and outcomes have been correlated with certain microbial taxa present in the host gut.

D. melanogaster serves as a useful tool for studying this relationship because its microbiota contains relatively few bacterial strains and is both widely studied and largely understood. Previous research within our lab involving D. melanogaster has found trends in many life-history strategies (ie. reproduction, fecundity, lifespan) that correlate with the presence of certain gut bacteria. While there are many aspects of health that microbiota composition affects, there are also a variety of factors that impact microbiota composition thus leading to these end results.

This experiment seeks to further understand the role that environment has in determining microbiota composition. By rearing gnotobiotic flies in environments that differ in temperature, we can then analyze microbiota content to see if any fluctuations occur due to environmental temperature. If temperature is found to have an effect on the taxa present in fully developed D. melanogaster, we can then seek to determine whether or not there are evolutions taking place in host genotype that yield differing microbiota phenotypically.

Thornton, Sherie; Cardona,Rebecca (Weber State University)
Faculty Advisor: Culumber, Michele (Weber State University, Microbiology); Oberg, Craig (Weber State University, Microbiology)

Lactobacillus wasatchensis was initially isolated from cheese produced at Utah State University and was found to be a Non-Starter Lactic Acid Bacteria (NSLAB) that causes late-gas production in cheese that can damage packaging and produce defects in the cheese. The goal of this project was to locate an environmental reservoir for Lactobacillus wasatchensis. Five samples of silage that were in different stages of fermentation and content and raw milk samples were obtained at the Utah State University dairy. Samples were serially diluted, plated on de Man, Rogosa and Sharpe agar supplemented with 1% D-Ribose (NRS-R) and incubated anaerobically for 5 days. Colonies that looked like potential Lb. wasatchensis were selected and regrown for isolation. All isolates were gram-positive rods. The isolates were further grown in broth for DNA extraction, sequencing, and analysis with API 50 carbohydrate panel (API 50CH). The API 50CH results were significantly different from Lb. wasatchensis, which only demonstrates use of ribose in this assay. Sequencing of the 16S rRNA gene, however, produced a match to three isolates from two different silage samples that had 99% sequence identity to Lb. wasatchensis. Further analysis of the isolates is being done to confirm this finding and describe the organism isolated from the soil. We hypothesize that these organisms are very closely related to Lb. wasatchensis and that silage could be an environmental source of contamination.

Hendricks, Kyle; Tessem, Jeffery (Brigham Young University)
Faculty Advisor: Tessem, Jeffery (Brigham Young University; Nutrition, Dietetics, and Food Science)

Over 30 million Americans suffer from type 1 (T1D) or type 2 diabetes (T2D), the seventh leading cause of death in the US. T1D and T2D is caused by a significant decrease in pancreatic β-cell mass, resulting in the body's inability to regulate blood glucose. Specifically, T1D is classified as an autoimmune disease due to pancreatic β-cell death by the body's T cells. Nf-κB is required for T cell mediated β-cell destruction. Nf-κB interacts with ICAM-1 on the T cell and acts in conjunction with IL-1β which acts as a T cell activator. This pathway is part of the mechanism that contributes to T cell mediated cell destruction. Here we hypothesize that IL-1β is involved in the mechanism that contributes to Nf-κB and ICAM-1 binding. We will begin with an electrophoretic mobility shift assay to identify the interactions between the ICAM-1 site on IL-1β treated cells and the Nf-κB binding complex. A better understanding of this pathology can, in the future, lead to a treatment that could regulate T cell mediated death of β-cells.