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Life Sciences

Bat Diversity and Habitat Preference in Southern Utah

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Author(s): Ammon Miles, Anthony Kemp, Connor Baty

CRISPR Deletion of Viral Receptor Genes in Human Cells

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Authors: Rylan Schmanski, Mason Masters, Emilee Snow, Alexandria Offringa, Paola Robles, Spencer Perry, Joshua Mackley, Alexander Beagley, Rainey Hughes. Mentors: Daniel Clark. Insitution: Weber State University. Enterovirus 71 (EV71) and herpes simplex 1 (HSV-1) are viruses that cause skin lesions in humans. EV71 causes hand foot and mouth disease (HFMD) and primarily affects young children. HSV-1 is a lifelong infection, causing genital herpes and cold sores, which affects 50 to 80 percent of US adults. We used CRISPR to edit the human genome in cultured cells (HEK293 and HeLa) to decrease the infectivity of these two viruses by deleting their receptors. To delete these virus receptors, a guide RNA (gRNA) was designed for each receptor using the Broad Institute gRNA design tool (ANXA2, SCARB2, and SELPLG for EV71, and Nectin-1 and HVEM for HSV-1). Plasmids that express each gRNA and the CRISPR cutting enzyme, Cas9, were transfected into human cells using the base plasmid All_in_one_CRISPR. This plasmid contains a dsRed fluorescent protein and a G418-selectable marker for the selection of transfected cells, which were then confirmed as knockouts by Sanger sequencing. Cells were then infected and compared for viral-induced apoptosis. Because viruses use combinations of receptors, the end goal is to determine which receptors are most critical for attachment and entry into human cells. This will lead to targeted antiviral drugs to block interactions with those receptors.

Bloom Buster: Engineering Chlamydomonas reinhardtii to combat toxic algal blooms

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Author(s): Erick Alvarez, Jonathan Kinross, Callie Ross, Pedro Rodriguez, Gerardo Acosta, Elise Bennett

Measuring the Efficacy of Various Test Anxiety Reducing Methods

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Author(s): Amber Best, Makenzie Porter, Kenna Olaya, Rachel Chapman

Brassicaceae of the Utah Valley

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Author(s): Gideon Bowes

Cannabis and the Mind: A Review of the Bidirectional Relations with Depression and Anxiety

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Author(s): Michael Coover, Ives Hong, Mattison Hillin, Hallee Hassell, Andrew Shepard

Generation and Characterization of a zebrafish 4H Leukodystrophy model

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Authors: Avery Zentner. Mentors: Hung Yu Shih. Insitution: Utah Tech University. 4H Leukodystrophy (4H) is an early-onset rare genetic disease, which causes myelination loss in the nervous system without a current cure. 4H patients exhibit different phenotypic spectrums of hypomyelination, hypodontia, and hypogonadotropic hypogonadism. Mutations in polr3a, polr3b, polr3k, and polr1c, which encode the RNA polymerase III subunits, could lead to 4H development. To date, there are no available animal models to bona fide the clinical symptoms of human patients, limiting the therapeutic development of 4H. Zebrafish, Danio rerio, might be an ideal model for 4H. Zebrafish have been widely used for human disease models and drug development. This project aims to establish and characterize the zebrafish 4H model by knocking out the polr3a with the CRISPR/Cas9 approach. The polr3a-Crispants significantly increased the mortality rate as compared to wild-type embryos. Behavior analysis showed the polr3a-Crispants reduced swimming ability upon light stimulation, which might reflect the clinical ataxia or vision problem. Quantitative PCR (qPCR) analysis showed a significant reduction in myelin-associated genes. These results suggest the polr3a knockout could mimic the clinical symptoms. Future studies will characterize the detailed neurological defects and the underlying mechanisms of 4H development and progression. Moreover, we will utilize the 4H zebrafish model for therapeutic drug screening.

Mechanism of Histidine Ammonia Lyase (HAL)

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Author(s): Romina Peralta, Isabel Amaro, Jessica Munro

The Role of Sirt7 in Beta Cell Function and Insulin Secretion

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Authors: Trevor Kendrick, Jakob Lenker. Mentors: Jeff Tessem. Insitution: Brigham Young University. Diabetes is a chronic metabolic disease characterized by an inability of beta cells to produce or secrete insulin due to decreasing beta cell mass, a condition induced by beta cell death or overuse. Current treatment consists of daily administration of insulin to diabetic individuals. We have shown that Sirtuin 7 (Sirt7), a deacetylase located in the nucleus, directly interacts with Nkx6.1, a transcription factor essential for beta cell function and proliferation. We have shown that one of the post translational modifications that impinges on Nkx6.1 activity is acetylation. Given Sirt7’s role as a deacetylase, and published reports demonstrating its impact on glucose stimulated insulin secretion (GSIS), we hypothesized that the interaction between Nkx6.1 and Sirt7 maybe needed for the Nkx6.1 mediated enhancement of glucose stimulated insulin secretion. Here we present data regarding the interaction between Nkx6.1 and Sirt7 in terms of Nkx6.1 acetylation status, effect on GSIS, and the effect of cultured glucose concentration on this interaction. These findings may be leveraged to develop interventions to better treat patients with type 1 and type 2 diabetes.

Enhancing Human Anatomy Education with Virtual Reality

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Author(s): Caleb Hoffman, Remi Cummings

Investigating the Mechanism of Histidine Ammonia Lyase (HAL)

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Author(s): Kordell Welch, Adam Jones, Taylor Strain, Andrew Martineau