Type: Undergraduate
Author(s): Nia Chambers Biology
Advisor(s): Giri Akkaraju Biology
Location: SecondFloor, Table 8, Position 1, 11:30-1:30

Chronic 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.

Expanding the Potential for Bacteriophage Therapy: Isolation of Phages against ESKAPE Pathogens

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

Expanding 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.

Investigating the effects of patient variants and phosphorylation on the BRCA1/PALB2 interaction

Type: Undergraduate
Author(s): Audrey Dolt Biology Chrissy Baker Biology Precious Castillo Biology Hayes Martin Biology Jamison Speed Biology Mikaela Stewart Biology
Advisor(s): Mikaela Stewart Biology
Location: Basement, Table 11, Position 1, 11:30-1:30

BRCA1 and PALB2 proteins suppress tumor formation by promoting homologous recombination when DNA damage has occurred. Mutations in BRCA1 and PALB2 are associated with a higher prevalence of breast and ovarian cancers. It is established that phosphorylation of BRCA1 and PALB2 occurs in or near the coiled-coil region of both proteins. This domain is utilized by both proteins to heterodimerize, so we hypothesize that phosphorylation events could affect BRCA1/PALB2 interaction affinity. We are using Isothermal Titration Calorimetry and Circular Dichroism to determine if phosphorylation affects the structure or function of minimized binding domains from BRCA1 and PALB2. We will present our findings from the PALB2 phosphorylation sites which, contrary to our hypothesis, do not affect binding to BRCA1, as well as forthcoming data on the BRCA1 phosphorylation sites. In addition, we are using the minimized constructs and similar techniques to study questions regarding the effect of variants of unknown significance on the structure and function of these regions. While we have many variants remaining to test, thus far we find that the coiled-coil structure is destabilized by the introduction of proline variants in particular; therefore these variants disrupt the binding between PALB2 and BRCA1 and are more likely to be detrimental. We will present a summary of the variants tested to date and our working hypothesis regarding structure and function disruptions in the coiled-coil domains of BRCA1 and PALB2.

The impact of novel Alzheimer’s Disease therapeutics on the activation of the pro-inflammatory transcription factor NF-ⲕB

Type: Undergraduate
Author(s): Lal Durmaz Biology
Advisor(s): Giridhar Akkaraju Biology
Location: Third Floor, Table 3, Position 3, 1:45-3:45

Inflammation is a natural and beneficial response to injury and pathogen invasion. However, chronic inflammation is linked to the progression of various neurodegenerative diseases. Although the exact etiology is unknown, Alzheimer’s disease is associated with the overactivation of the NF-kB inflammatory pathway. NF-kB is a transcription factor that, in an unstimulated cell, is sequestered in the cytoplasm as a complex with its inhibitor, IκBα. When the pathway is activated by an external signal, IκBα is phosphorylated and subsequently degraded in the proteasome. Liberated NF-κB translocates to the nucleus, where it acts as a transcription factor for pro-inflammatory genes, highlighting its potential as a therapeutic target. Our research investigates the exact point of interference of novel anti-inflammatory drugs (provided by P2D Biosciences) with the NF-kB pathway through Western blotting and immunofluorescence.

Characterizing a C. elegans Model for Oxidative Stress Response

Type: Undergraduate
Author(s): Nicholas Findlater Biology Madelynn Farhat Biology
Advisor(s): Thushara Galbadage Interdisciplinary Giridhar Akkaraju Biology
Location: SecondFloor, Table 9, Position 1, 11:30-1:30

Neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease are characterized by progressive neuronal loss, often driven by oxidative stress. The accumulation of reactive oxygen species (ROS) contributes to cellular damage, making oxidative stress a key factor in disease pathology. Caenorhabditis elegans, a genetically tractable model with conserved stress response pathways and neuronal structures, provides an effective system for studying oxidative stress and neurodegeneration. This study aims to establish an optimized oxidative stress assay in C. elegans to evaluate protective effects against ROS-induced damage. Wild-type (N2) C. elegans were synchronized via a bleaching protocol to generate a uniform population of young adults. Lifespan and survival assays were performed using tert-butyl hydroperoxide (tBHP) to induce oxidative stress, testing concentrations of 10, 1, 0.1, and 0.01 mM. Higher concentrations (10 and 1 mM) resulted in rapid mortality of C. elegans within 3 and 9 hours, respectively, whereas lower concentrations (0.1 and 0.01 mM) allowed survival beyond 12 hours. Based on these findings, an optimal tBHP concentration will be used to further refine this oxidative stress model. This study provides foundational data for investigating the efficacy of potential antioxidant molecules in reducing ROS-related damage. By using the C. elegans model, future research will focus on identifying molecular mechanisms of oxidative stress response and evaluating therapeutic candidates for neurodegenerative diseases.