BIOL2025BOEHLY47210 BIOL
Type: Undergraduate
Author(s):
Nicholas Boehly
Biology
Bridey Brown
Biology
Emersyn Jorski
Biology
Advisor(s):
Dr Matthew Hale
Biology
Location: SecondFloor, Table 9, Position 1, 1:45-3:45
View PresentationNick Boehly, Bridey Brown, Emersyn Jorski, Matthew Hale
Texas Christian University, Department of Biology
Previous studies have shown that nutrition plays a key role in influencing epigenetic markers. Additionally, changes in gene expression have been linked to the development of Alzheimer’s disease (AD). However, it is unclear how, and to what effect, nutrition influences changes in the epigenome. To that end, we divided mice into groups and exposed them to two different diets 1) a typical American diet (TAD) and 2) a Mediterranean diet (MD). Although it is known that diet can induce epigenetic modification, it is unknown if these changes are heritable. There has been little research that has focused on the offspring of the mice fed with these diets. Therefore, this experiment will focus on how the diets of parental mice affect their offspring’s methylation patterns of previously identified candidate genes linked to the development of AD. Prefrontal cortex samples from F1 mice, whose parents were exposed to MD or TAD, were removed, and the RNA was extracted and reverse transcribed into cDNA. This cDNA will display levels of expression by 10 distinct genes that have been linked to AD in previous studies. Our goal is to identify correlations between nutrition and the development of AD through modifications of gene expression. Moreover, this data will help illustrate how inheritance of epigenetic modifications can influence gene expression in subsequent generations.
BIOL2025CARLTON20951 BIOL
Type: Undergraduate
Author(s):
Drew Carlton
Biology
Dalton Allen
Biology
Marlo Jeffries
Biology
Katie Solomons
Biology
Reagan Spickard
Biology
Advisor(s):
Marlo Jeffries
Biology
Location: Basement, Table 15, Position 2, 1:45-3:45
View PresentationThe Trinity River is an important body of water to the state of Texas as it is a source of drinking water for the Dallas-Fort Worth and Houston Metropolitan areas, a popular location for recreational activities, and an ecologically significant habitat for a variety of organisms. Due to its urban location, the Trinity River is subject to potential heavy metal pollution from wastewater treatment plant discharge, road runoff, and industrial activities. Heavy metal exposure has been shown to cause significant adverse impacts on aquatic organisms; thus, this project aimed to evaluate the presence and biological impact of heavy metals in sediment and surface water samples collected from the Trinity River. Water samples collected from the Trinity River were tested for the presence of heavy metals using ICP-OES. Larval fathead minnows were also exposed to sediment and surface water samples collected from the Trinity River and gene expression levels of five biomarkers were measured. Metallothionein was used as a biomarker of exposure to heavy metals, catalase and superoxide dismutase were used as biomarkers of oxidative stress, and heat shock proteins 70 and 90 were used as biomarkers of generalized stress. The results of this study provide insight into the extent of heavy metal contamination in the Trinity River, as well as its potential impact on aquatic life.
BIOL2025CHADWICK36742 BIOL
Type: Undergraduate
Author(s):
Braden Chadwick
Biology
Alex Caron
Biology
Sheridan O'Coyne
Biology
Katherine Richey
Biology
Mikaela Stewart
Biology
Advisor(s):
Shauna McGillivray
Biology
Location: Basement, Table 15, Position 1, 11:30-1:30
View PresentationAs increasing antimicrobial resistance continues to limit treatment options for bacterial infections, several new approaches have sought to avoid the challenges faced by traditional antibiotics. One such approach is targeting virulence factors, which are necessary for pathogens to evade host defenses and establish infection but not for survival outside the host. This strategy could provide an effective form of treatment while reducing selective pressures for bacteria to evolve resistance mechanisms. Studies have shown that the ClpXP proteolytic complex is essential for virulence in Bacillus anthracis and that deletion of the ClpX subunit increases sensitivity to the cell-envelope-targeting antibiotics penicillin and daptomycin as well as the human antimicrobial peptide LL-37. Previously, we used computational modeling to identify commercially available inhibitors of the ClpXP complex and demonstrated that one, ritanserin, mimics the phenotype of a B. anthracis ΔclpX knockout mutant in antimicrobial susceptibility assays. In this study, we evaluated ritanserin in comparison to four other inhibitors identified during the same screen—siramesine, xaliproden, fluspirilene, and R59022—by determining the fractional inhibitory concentration (FIC) index of each when used in combination with penicillin. Notably, all inhibitors used except R59022 have undergone at least phase II clinical trials for other purposes. We found that two out of the three inhibitors with the highest predicted binding affinity, ritanserin and siramesine, exhibited synergistic interaction with penicillin, while the remainder of the interactions were indifferent. Our results further demonstrate the potential of structural biology techniques to identify and repurpose existing drugs for use as novel antibiotics.
BIOL2025CHAMBERS17534 BIOL
Type: Undergraduate
Author(s):
Nia Chambers
Biology
Advisor(s):
Giri Akkaraju
Biology
Location: SecondFloor, Table 8, Position 1, 11:30-1:30
View PresentationChronic inflammation is a major contributor to neurological damage in diseases such as Alzheimer’s, which currently affects nearly 7 million Americans. The NF-kB signaling pathway plays a critical role in mediating inflammatory responses, as it regulates the expression of several pro-inflammatory cytokines, such as TNF-alpha, that exacerbate neuroinflammation. This study investigates the effectiveness of novel compounds in regulating TNF-alpha induced NFkB activation, using a luciferase reporter assay.
BIOL2025CRONK60206 BIOL
Type: Undergraduate
Author(s):
Sophie Cronk
Biology
Cassidy Hunter
Biology
Katherine Lesslie Lesslie
Biology
Aeron Pennington
Biology
Advisor(s):
Shauna McGillivray
Biology
Location: Third Floor, Table 5, Position 1, 11:30-1:30
View PresentationExpanding the Potential for Bacteriophage Therapy: Isolation of Phages against ESKAPE Pathogens
Sophie Cronk, Katherine Lesslie, Cassidy Hunter, Aeron Pennington, Shauna M McGillivray
Bacteriophages are viruses that selectively infect bacteria and propagate to overtake the host species.
They are also being developed as a treatment for otherwise drug-resistant infections. Though
bacteriophage therapy has not been FDA approved; it has been used in cases of compassionate care.
Because of the success in these cases, bacteriophage is offering a promising alternative to antibiotics
in the fight against antibiotic resistance. One issue in mainstream bacteriophage use is them
selectivity. Phages infect a specific bacterial species or a particular strain within the species.
Therefore, multiple phages may be required in a ‘phage cocktail’ to ensure there is a phage infects a
target bacterial strain. The goal of our bacteriophage study was to gather data about
where phages are heavily populated and to refine protocols to ensure optimal bacteriophage
collection. Bacteriophage that attacks different bacterial hosts tends to be found in locations
that commonly accumulates that specific host bacteria. A secondary goal is to isolate as many phages as
possible against bacterial species known as the ESKAPE pathogens. The ESKAPE pathogens are Staphylococcus aureus, Enterobacter
aerogenes, Pseudomonas aeruginosa and Klebsiella pneumoniae. These are clinically relevant
because their antibiotic resistance poses a threat to public health due to their ability to cause severe
infections. We have successfully isolated bacteriophage for Pseudomonas aeruginosa, Klebsiella,
and Enterobacter and we are actively exploring different environments for phage that will infect
S. aureus.