Investigating the Effects of Peptide Mimics on the Binding Interaction between BRCA1 and PALB2

Type: Undergraduate
Author(s): Madison Adam Biology
Advisor(s): Mikaela Stewart Biology

Thermal Tolerance and Reproductive Responses of Northern and Southern Dreissena polymorpha Populations

Type: Undergraduate
Author(s): Madeline Comeaux Biology
Advisor(s): Michael Misamore Biology

Determination of gamete viability in dreissenid zebra and quagga mussels

Type: Undergraduate
Author(s): Molly Corriere Biology
Advisor(s): Mike Misamore Biology

Novel Drivers of Nest-site Selection in Texas Horned Lizards

Type: Graduate
Author(s): Kira Gangbin Biology Julianne Li Interdisciplinary Madison Upton Interdisciplinary Dean Williams Biology Brian Wright Interdisciplinary
Advisor(s): Dean Williams Biology

Reproductive success in oviparous reptiles is shaped by both nest environment and post-emergence resource availability. While the abiotic conditions of a reptile’s nest can greatly influence hatching success, post-emergence resource availability affects hatchling survival and growth. Many studies evaluate whether females favor particular nesting sites based on abiotic conditions; however no studies have linked nest site choice with post-emergence resource availability. Understanding this relationship could improve habitat management and enhance survival in Texas horned lizard (Phrynosoma cornutum) reintroduction programs. The species’ strong dietary specialization, particularly the reliance of hatchlings on small native ants (Crematogaster, Dorymyrmex, Pheidole, and Tetramorium spp.), makes it possible to test whether females select nest sites that maximize post-emergence prey availability. During the summers of 2023 and 2024, we located 21 nests of Texas horned lizards at a reintroduction site at Mason Mountain WMA and at a natural population (~42 km away) in central Texas. We compared nest and random sites to assess a female’s ability to select a nest site based on fire ant abundance, native ant abundance, soil moisture, soil compaction, and vegetation structure. Using stepwise model selection, results suggest that horned lizards select nest sites that have low soil compaction, reduced grass cover, and high amounts of hatchling prey. This information will be used to determine if there are suitable nesting areas at reintroduction sites and how to best manage land for optimum horned lizard survival. Release sites with softer soil, less grass, and higher abundance of native ants should be prioritized.

The Effect of Media Type on ZnO Cytotoxicity

Type: Undergraduate
Author(s): Louise Hutchison Biology
Advisor(s): Shauna McGillivray Biology Yuri Strzhemechny Physics & Astronomy

The increasing prevalence of antibiotic-resistant bacteria, including Staphylococcus aureus, has intensified the search for alternative antimicrobial strategies. Metal oxides have emerged as promising candidates, with zinc oxide (ZnO) attracting particular interest due to its low cost, thermal and mechanical stability, and minimal generation of harmful by-products. ZnO has potential applications in medical device coatings, food preservation, and topical therapeutics. Previous work in our laboratory demonstrated that growth inhibition of S. aureus correlates with the release of Zn²⁺ ions from ZnO Sigma particles in Mueller–Hinton broth (MHB) (Caron et al., 2024). However, it has been reported that the media can influence Zn2+ dissolution and ZnO toxicity. In support of this, we find that ZnO particles exhibit increased dissolution in saline compared to MHB, resulting in enhanced cytotoxicity toward S. aureus. To further investigate the influence of different media types on ZnO dissolution and bacterial survival, we will investigate HEPES and MOPS buffers as media alternatives to assess ZnO toxicity. By evaluating how different chemical environments affect Zn²⁺ release and antimicrobial activity, this work aims to maximize the potential of ZnO-mediated cytotoxicity.

Investigating the Role of Core Gut Symbionts in Defending Bumble Bees Against Opportunistic Pathogens

Type: Undergraduate
Author(s): Dylan Masson Biology
Advisor(s): Annika Nelson Biology

Using genomics to determine origins and dispersal patterns of invasive northern pike (Esox lucius) in southcentral Alaska

Type: Graduate
Author(s): Mikay Reuter Biology
Advisor(s): Matthew Hale Biology

Invasive species harm local ecosystems, economies, and cultures. There has been a substantial effort to research the recent increase in the number and frequency of successful invaders; however, relatively little information regarding if and to what extent genetics influences a species ability to become a successful invader exists. Whole genome sequencing provides a mechanism that could illuminate the importance of genetics for successful invasion and uncover the roles selection plays in predisposing populations to be successful invaders. Northern pike (Esox lucius) are native to the Holarctic region but have been widely introduced across Europe and North America. For example, pike were introduced to the area around Anchorage, Alaska in the 1970s and have since spread throughout southcentral Alaska. This species represents a major threat to populations of native fish species, especially multiple species of salmonid. Current management efforts appear to fall short as many pike populations have increased following removal. Part of this growth is likely from the ability of pike to disperse into marine environments, allowing them to colonize new bodies of freshwater. However, whether this ability to disperse is genetic – and therefore heritable - remains unknown. If there are alleles that predispose some populations of pike to be successful invaders, then such populations should be the target of multifaceted eradication efforts. To that end, several populations of pike – consisting of known residents and dispersers - from south-central Alaska were analyzed using whole genome sequencing to a) determine if there are alleles associated with dispersal ability and b) to determine if and to what extent populations are predisposed to dispersal behaviors. Overall, this research will improve our understanding of the genetic basis of invasive biology, identify populations of pike that should become a priority for eradication, and help protect native fish species.

Genetic Analysis of Captive-Bred Texas Horned Lizards (Phrynosoma cornutum)

Type: Undergraduate
Author(s): Alexis Winter Biology
Advisor(s): Dean Williams Biology

Endocrine Disruption Screening: Can Vertebrate Endocrine Disruptors Impact Invertebrate Molting?

Type: Graduate
Author(s): Dalton Allen Biology Justin Hunt Biology Marlo Jeffries Biology Laurel Skrnich Biology
Advisor(s): Marlo Jeffries Biology
Location: Basement, Table 9, Position 1, 1:45-3:45

Mysid shrimp (Americamysis bahia) have been utilized in routine marine toxicity assessments for decades. While mysids are a well-established model, there a key gaps in understanding how chemical exposure impacts their endocrine systems. Crustacean growth occurs through molting (i.e., shedding old exoskeleton), a process regulated by hormones, primarily ecdysteroids. Ecdysteroids are a class of steroid hormones that share similar chemical structures to vertebrate hormones (i.e., 17β-estradiol and testosterone), which have been suggested to disrupt molting in some invertebrates. Through powerful tools, like transcriptomics, potential genetic biomarkers may be identified following chemical exposure. These biomarkers could provide the basis for future research aimed at screening endocrine disrupting compounds using invertebrate models. The objectives of this work were to 1) assess whether known vertebrate endocrine disruptors (e.g., 17β-estradiol and trenbolone) would induce alterations in molting and growth and, 2) compare gene expression profiles between vertebrate endocrine disruptors and a model ecdysteroid (i.e., ponasterone A) using transcriptomic analysis. Ponasterone A induced predictable alterations in mass, molting, and ecdysteroid-related gene expression, reinforcing both the use of this compound as a positive control and these endpoints for assessing invertebrate endocrine disruptors. Vertebrate endocrine disruptors induced varied responses in the endpoints assessed, but neither acted in a manner comparable to ponasterone A. Future work may investigate the potential for differentially expressed genes identified in the transcriptomic analysis for screening of invertebrate endocrine disruptors.

Investigating diet-induced metabolic syndrome in a typical American versus Mediterranean diet model in C57Bl/6J mice

Type: Graduate
Author(s): Morgan Bertrand Biology Gary Boehm Psychology Logun Gunderson Psychology
Advisor(s): Michael Chumley Biology
Location: SecondFloor, Table 6, Position 2, 11:30-1:30

Metabolic syndrome (MetS) is a cluster of concurrent cardiometabolic risk factors, including increased waist circumference, hypertension, elevated triglyceride level, reduced high-density lipoprotein (HDL) cholesterol level, and hyperglycemia. The key pathophysiology of MetS is insulin resistance, resulting in a disruption of glucose and lipid metabolism in the liver and adipose tissue, which increases the risk of type II diabetes, cardiovascular disease, and stroke. The development of insulin resistance and related conditions is multifaceted, but risk can be mitigated with lifestyle modifications, including improved nutrition. In the US, a typical American diet (TAD) is full of highly processed foods high in saturated fats and refined sugars and is associated with increased insulin resistance and obesity risk. In contrast, adherence to a plant-based Mediterranean diet (MD) rich in unsaturated fats, fiber, and non-refined carbohydrates has been found to reduce disease risk. Despite the contrasting nutritional compositions, the average macronutrient distributions of these two human diet styles are similar (approximately 50% kcal carbohydrates, 15% kcal protein, and 35% kcal fat). Due to the comparable macronutrient ratios but contrasting nutritional composition, direct comparative analysis could uncover metabolic and cellular differences relating to their associated health outcomes.

There are few rodent studies in the literature that directly compare a TAD and MD. Further, studies often utilize a high-fat diet, consisting of 40-60% kcal fat, or individual nutrient supplements, such as olive oil, rather than comprehensive diet models. To address these limitations, our lab developed comprehensive, macronutrient-matched TAD and MD models that more closely mimic human diets in the U.S. and Mediterranean, respectively. A previous study in our lab found that six months of TAD consumption resulted in elevated body weight, increased inflammation, and excess hepatic lipid deposition, in comparison to the MD. Our current study looked to further characterize MetS under this diet model, specifically investigating obesity, insulin resistance, and dyslipidemia markers. Male and female C57BL/6J mice consumed either the TAD or MD from the age of 4 to 7 months. We found that after three months on diet, there were elevations in hepatic steatosis and serum cholesterol levels in both males and females on the TAD. However, other findings suggested early signs of insulin resistance in TAD males, but not females. Future studies will investigate MetS after 6 months on diet to better elucidate insulin resistance development and potential sex differences.

Effects of Parental Diet on the Offspring's Epigenome and Expression of Genes Associated With Alzheimer's Disease

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

Nick 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.

Investigation of the Presence and Impact of Heavy Metals in the Trinity River

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

The 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.

Efficacy of Repurposed ClpXP Protease Inhibitors in Bacillus anthracis Sterne Strain

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

As 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.

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.

Genetic Variation in Alligator Weed Influences Herbicide Effectiveness Across Regions

Type: Undergraduate
Author(s): Namandeep Gill Biology Dean Williams Biology
Advisor(s): Dean Williams Biology
Location: Basement, Table 2, Position 3, 11:30-1:30

Alligator weed (Alternanthera philoxeroides) is a highly invasive species that threatens waterways, agriculture, and ecosystems worldwide. While herbicide treatments have successfully managed populations in Mississippi, they have been less effective in Australia and New Zealand. This research investigated whether genetic differences among populations contribute to these inconsistencies in control effectiveness. To test this, we genotyped alligator weed samples from Mississippi, Australia, and New Zealand using chloroplast DNA markers to identify haplotypes. Results revealed significant genetic variation among regions. Mississippi populations exhibited greater haplotype diversity, with Ap1 and Ap3 being dominant, whereas Australia and New Zealand were primarily composed of Ap2, Ap3, and Ap5. The genetic lineages used in Mississippi herbicide trials did not directly match those found in Australia and New Zealand, suggesting that differences in herbicide response may be linked to genetic variation. These findings indicate that current herbicide trials may not accurately predict effectiveness in non-U.S. regions. Future testing on genetically relevant populations will improve control strategies, ensuring more effective management of alligator weed globally.

EmpowerHer STEM Club

Type: Undergraduate
Author(s): Lilli Gonzales Biology Daisy Carrillo Environmental Sciences Hermela Leul Nutritional Sciences Zoie Munoz Dean's office Kelley Wyatt Biology
Advisor(s): Christina Ayala Biology
Location: SecondFloor, Table 1, Position 1, 1:45-3:45

EmpowerHer STEM Club is an after-school program dedicated to encouraging young girls to explore careers in science, technology, engineering, and mathematics (STEM). In collaboration with E.M. Daggett Elementary School, the program seeks to address the gender gap in STEM fields, where women currently hold only 28% of STEM occupations. Research suggests that early mentorship plays a crucial role in shaping young women's academic and career aspirations.
EmpowerHer STEM Club provides mentorship and hands-on learning experiences to inspire and support young girls in their STEM interests. The program introduces students to diverse STEM fields through interactive experiments that complement their classroom curriculum. Additionally, participants learn about various STEM careers and the achievements of influential women in these fields. Through this engaging approach, EmpowerHer STEM Club fosters curiosity, confidence, and a passion for STEM while building connections with the next generation of leaders.

The Effects of Novel Anti-Inflammatory Drugs on LPS-Induced Cytokine Gene Expression in BV2 Cells

Type: Undergraduate
Author(s): Ana Herget Biology Giridhar Akkaraju Biology
Advisor(s): Giridhar Akkaraju Biology
Location: Basement, Table 7, Position 3, 1:45-3:45

Alzheimer’s Disease (AD), the most common form of dementia, currently impacts almost seven million people in the United States over the age of 65. It is predicted that by 2060 over 13 million people in the United States will be affected by AD, which is why there is a growing demand for treatments. Amyloid ꞵ plaques and phosphorylated tau proteins are both associated with the progression of the AD pathology since they play a role in the disruption of neuronal integrity. These aggregated proteins along with other molecules, such as lipopolysaccharide (LPS), lead to increased inflammation by activating the NFκB pathway. The NFκB pathway controls the production of pro-inflammatory cytokines, such as interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNFɑ); however, if it is overactive, it can lead to harmful inflammation.The company P2D Biosciences provides novel compounds designed to reduce inflammation, but the exact mode of action of these compounds is unknown. Quantitative reverse transcription polymerase chain reaction (RT-qPCR) can be utilized to measure cytokine mRNA from BV2 cells that have been pretreated with the drugs and then with LPS. In this project we screened multiple compounds provided by P2D Biosciences to evaluate their use as anti-inflammatory agents to treat AD.

Investigating the ubiquitin ligase activity of BRCA1 from C. elegans

Type: Undergraduate
Author(s): Lauren Herrington Biology
Advisor(s): Mikaela Stewart Biology
Location: Third Floor, Table 8, Position 1, 1:45-3:45

BRCA1 is a tumor suppressor protein that normally acts with its partner, BARD1, to facilitate DNA repair, regulation of the cell cycle, and regulation of gene expression. The Caenorhabditis elegans homologs of BRCA1 and BARD1, BRC-1 and BRD-1, respectively, retain these key functions and thus make C. elegans a suitable model organism for studying the functions of BRCA1. While the functions of BRCA1 and BRC-1 are well characterized, the molecular mechanisms by which these functions are carried out is still unclear. For example, BRCA1 and BRC-1 possess E3 ubiquitin ligase activity towards histone H2A in nucleosomes, but it is unknown how this contributes to tumor suppression. While inherited mutations that disrupt tumor suppression lack E3 ligase activity, they also interfere with other critical molecular functions, such as BARD1 binding. To pinpoint the role of E3 ligase activity, we aim to characterize a mutant construct of BRC-1 in C. elegans that lacks E3 ubiquitin ligase activity towards histone H2A but retains the ability to bind BRD-1. In vitro ubiquitination assays demonstrate that our candidate for this mutant of BRC-1, Trip A, is ligase-dead towards histone H2A in nucleosomes. Co-purification of BRC-1 and BRD-1 in which only BRC-1 contained the histidine tag revealed that BRC-1:BRD-1 binding is retained in the Trip A mutant. While these results demonstrate that Trip A meets in vitro requirements for a ligase-dead mutant, further in vivo experiments are needed to confirm its suitability. If confirmed as a suitable ligase-dead mutant through in vivo experiments, Trip A can be expressed in C. elegans to identify which functions of BRC-1 depend on E3 ubiquitin ligase activity towards histone H2A in nucleosomes.

Identifying the nucleosome ubiquitylation role of BRCA1 in transcriptional regulation using C. elegans

Type: Undergraduate
Author(s): Elizabeth Hoff Biology
Advisor(s): Mikaela Stewart Biology
Location: FirstFloor, Table 1, Position 1, 1:45-3:45

BRCA1 is a tumor suppressor protein that facilitates DNA damage repair, cell cycle checkpoints, and gene expression in humans. The presence of pathogenic mutations in the BRCA1 protein leads to a predisposition to breast and ovarian cancers in humans; these pathogenic mutations can lead to the dysregulation of enzymatic activity and gene expression. It is hypothesized that enzymatic activity of BRCA1 and its ability to regulate gene expression are linked. The gene expression of estrogen-metabolism genes by BRCA1 is mediated, in-part, by the ability of BRCA1 to facilitate the mono-ubiquitylation of nucleosomes on the H2A histone. Our lab is interested in understanding which DNA damage repair and gene expression functions of BRCA1 rely on mononucleosome ubiquitylation. In Caenorhabditis elegans, the BRCA1 homolog, BRC-1, retains the key functions of BRCA1, making C. elegans a suitable model organism to evaluate which functions of BRCA1 rely on nucleosome ubiquitylation. To explore nucleosome ubiquitylation by BRC-1 in C. elegans, we compare three strains of C. elegans, including a wildtype strain, a complete knockout of BRC-1, and an engineered mutant. This engineered mutant contains two point mutations that alter the ability of BRC-1 to interact with the nucleosome to complete ubiquitylation of the H2A histone. We suggest that our proposed mutant repels BRC-1 from the histone to prevent ubiquitylation, yet retains all other BRC-1 functions. We hypothesize that this will hinder the repression of cyp genes, which code for enzymes that catalyze the process that converts estrogen into various metabolites, some of which are harmful. Overexpression of these genes can lead to the accumulation of harmful estrogen metabolites, which can lead to tumorigenesis in estrogen-metabolizing tissues. To assess this, we compare the expression levels of cyp genes, which are repressed in the wildtype strain containing a functional copy of BRC-1. If mononucleosome ubiquitylation is required for transcriptional repression in C. elegans, in the engineered mutant strain, we expect to see elevated levels of cyp gene expression, as also seen in the complete BRC-1 knockout strain. Through understanding the mono-ubiquitylation of nucleosomes by BRC-1 in C. elegans, we can better interpret the genetic variations of BRCA1 in humans and better inform and treat patients with detrimental BRCA1 mutations.

Trade-offs between environmental concerns and disease control influence disease dynamics across communities

Type: Undergraduate
Author(s): Redon Limani Biology Kenny Lai Biology Grant Xiong Biology
Advisor(s): Jing Jiao Biology
Location: Third Floor, Table 6, Position 2, 11:30-1:30

Mosquitoes are primary vectors in the transmission of many infectious diseases, spreading pathogens through their bites after feeding on infected
hosts. Vector-borne diseases like Zika, chikungunya, and yellow fever, mostly transmitted by mosquitoes, cause over 700,000 deaths each year and
account for 17% of infectious diseases, heavily burdening vulnerable communities and economies. Public perception of mosquito control can significantly shape outbreak outcomes [1]. This project uses a mathematical model to simulate how disease spreads between two regions connected by mosquito migration. The model considers how people’s concern for the environment can influence their support or opposition to mosquito control efforts. Our goal is to explore how these factors shape disease prevalence and to better understand the role of community behavior in outbreak prevention.

The enzymatic role of nucleosome ubiquitylation by BRCA1 in C. elegans

Type: Graduate
Author(s): Meagan McMann Biology Nathalie Carlon Biology Lucy McCollum Biology
Advisor(s): Mikaela Stewart Biology
Location: Third Floor, Table 1, Position 3, 1:45-3:45

BRCA1 protects genomic stability by signaling for the homologous recombination pathway, DNA repair, and transcriptional regulation. A pathogenic mutation in the BRCA1 region causes a higher predisposition to the development of breast and ovarian cancer. Our lab is exploring the different enzymatic functions of BRCA1 by looking at its role in histone ubiquitylation, leading to transcriptional regulation of certain parts of the genome. Join us to see our plan for connecting molecular mechanisms of a large, multi-functional gene to the phenotype of an organism. A homolog of BRCA1 is conserved in C. elegans as BRC-1. We propose that mononucleosome ubiquitylation is a key mechanism contributing to the cellular functions of BRC-1. Understanding the significance of mononucleosome ubiquitylation in BRC-1 with C. elegans gives insight into the mechanisms of genetic variations in BRCA1 and further expands C. elegans’ function as a model organism. We have generated a C. elegans mutant with two point mutations that alter the ability of BRC-1 protein to interact with the nucleosome and ubiquitinate histone H2A while retaining all other functions. We hypothesize this mutation increases DNA damage accumulation and disrupts transcriptional regulation to establish nucleosome ubiquitylation as a necessary precursor for these, but likely not all, BRC-1 functions. We compare three strains of C. elegans (wildtype, brc-1 knockout, and our mononucleosome ubiquitylation-deficient mutant) in different conditions designed to induce cellular stress or DNA damage accumulation. We find that BRC-1 nucleosome ubiquitylation contributes to embryonic survival under standard conditions as well as DNA damage-inducing conditions. We also share preliminary results regarding the role of nucleosome ubiquitylation in transcription regulation and reactive oxygen species generation. Our findings further the understanding of the many enzymatic functions of the large BRCA1 gene.