Alzheimer’s disease is the fastest growing form of dementia in the world. Currently the origin of disease is unknown, however, there are distinct signs seen in patients with Alzheimer’s disease (AD). Chronic neuroinflammation, increased ROS, dyshomeostasis of metal ions, Tau tangles, and mitochondrial dysfunction are well known to the pathogenesis and progression of this disease. Despite the pathogenesis being well documented, most current drugs treat symptoms of the disease, but have no effect on the progression of disease. The aim of this study is to test novel antioxidant compounds (L2 and L3) for their ability to reduce intracellular ROS in mice microglial cells (BV-2) and mice hippocampal cells (HT-22). DCFH-DA assays were used to measure the ROS levels. MTT assays were used to assess cell viability and determine safe concentrations of antioxidant compounds to use. Results of this study show significant reductions of ROS (TBHP) in BV-2 and HT-22 cells by L2, as determined by the DCFH-DA assay. These results are significant because it shows that L2 does not only protect neuronal cells from oxidative stress, but it can also decrease microglial inflammatory response.

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.

Zebra and quagga mussels originated in Eastern Europe and were introduced to the United States in the mid-1980s. After spreading from the Great Lakes throughout much of the eastern United States, including Texas, both species have become major ecological and economic pests. The objective of my project is to investigate the hybridization potential between two invasive dreissenid species, Dreissena polymorpha (sebra mussel) and Dreissena rostriformis begensis (quagga mussel). I will analyze fertilization, success, gamete compatibility, larval development, and competitive sperm binding to determine the success and viability of hybridization. Understanding this is important, as hybridization could increase genetic diversity, novel advantageous traits, and the potential for range expansion.

Bumblebees play a central role in pollinating both crops and natural plant populations. Yet, many bumblebee species are declining due to numerous anthropogenic effects, including exposure to pathogens. Bumble bees rely on a specialized community of gut bacteria, termed the “core” gut microbiome, to provide resistance against pathogens. However, the roles of particular bacterial species and strains within the core gut microbiome for defending against opportunistic pathogens remain unclear. This study investigated whether two abundant core gut bacteria – Gilliamella bombi and an unidentified bacterial strain isolated from bumble bee workers (Bombus impatiens) – reduce colonization by the opportunistic bacterial pathogen Serratia marcescens. After experimentally inoculating bumblebees with these two bacterial symbionts across a range of doses, we quantified bee resistance to pathogen infection by counting the number of colony-forming units (CFUs) of S. marcescens that colonized the gut. Contrary to expectations, the symbionts examined did not reduce pathogen colonization rate. These findings suggest that protection may require the full microbial community, specific combinations of taxa, or context-dependent interactions. Understanding when and how microbiomes confer defense is critical for predicting pollinator health under environmental change, and our research suggests that additional work is needed to identify probiotic bacteria that could be deployed to promote pollinator health.

BRCA1 protects genomic stability by signaling for the homologous recombination pathway, DNA repair, and transcriptional regulation. A pathogenic mutation in BRCA1 causes a higher predisposition to the development of breast and ovarian cancer. BRCA1 acts as a scaffold for many dynamic protein complexes, as well as functions as an E3 ligase towards various substrates. We do not know which if these interactions and substrates are tied to the many phenotypes associated with BRCA1 dysfunction. Our lab is exploring the importance of BRCA1 E3 ligase activity toward the substrate histone H2A. Using structural and biochemical assays we designed a BRCA1 mutant that maintains other critical BRCA1 interactions and substrates but specifically eliminates nucleosome ubiquitylation. This mutant allows us to connect this specific BRCA1 function to downstream phenotypes at an organismal level. A homolog of BRCA1 is conserved in C. elegans as BRC-1. We propose that nucleosome monoubiquitylation is a key mechanism contributing to some cellular functions of BRC-1, including DNA damage accumulation and transcriptional regulation of cytochrome p450 genes. We have generated a C. elegans mutant strain with these two specific point mutations that alter the ability of BRC-1 protein to interact with the nucleosome and ubiquitylate 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 nucleosome monoubiquitylation-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. Preliminary results also indicate an intermediate response regarding the role of nucleosome ubiquitylation in transcription regulation of cytochrome p450 genes. These findings help us better connect specific BRCA1 activity with downstream functions in the organism. We hope this project can be used as a blueprint for how protein structure to function relationships can be explored with the powerful C. elegans.

Iron Regulatory Proteins 1 and 2 (IRP1 and IRP2) are key regulators of cellular iron levels. Iron is essential for proper brain development and function, but can lead to cellular damage if not properly regulated. To investigate the effects of reduced expression of IRP1 and IRP2 on neuronal health and neurodegeneration, we are using mouse neurons that have been transfected with shRNA to specifically knock down IRP1 or IRP2. Mouse neurons are well-studied and share many key cellular pathways with human neurons, making them an appropriate model to study the effects of IRP1 and IRP2 knockdown. We will investigate the effect of the knockdowns on the mouse neurons through proliferation assays and differentiation assays. These experiments will reveal how the knockdown of IRP1 and IRP2 affects neuronal growth, maturation, and development compared to healthy control cells. Understanding these processes is incredibly important for humans, as iron dysregulation can lead to neurodegenerative diseases such as Alzheimer's.

The Arctic is contaminated with mercury (Hg) higher than historic baselines because of emissions from temperate and subtropical areas. The nonbioavailable form, inorganic Hg, is deposited on the landscape and is thought to have limited impacts on terrestrial organisms. In aquatic systems, inorganic Hg is converted to methylmercury (MeHg), a contaminant that biomagnifies through food webs and poses reproductive and neurological risks to wildlife and humans. The Arctic wolf spider (Pardosa glacialis), is one of the most abundant terrestrial predators in western Greenland, and prior research has linked MeHg concentrations in wolf spiders to emergent aquatic insects, indicating cross-ecosystem contaminant transfer. While freshwater ecosystems are recognized as important sources of MeHg to terrestrial consumers, recent observations suggest that Arctic terrestrial insects may also exhibit elevated Hg concentrations comparable to aquatic insects, potentially providing an additional pathway of contamination for terrestrial predators. However, the relative contribution of aquatic versus terrestrial prey to P. glacialis diets across Arctic ponds remains unclear. We investigated how aquatic and terrestrial prey contribute to the diet of P. glacialis and how this dietary composition may influence contaminant exposure in Arctic terrestrial food webs. We hypothesize that wolf spiders consume a mixture of both aquatic and terrestrial insects, broadening the source of P. glacialis’s contamination. To test this, we captured and analyzed wolf spiders, terrestrial insects, and emergent aquatic insects at six Arctic pond sites. Across all ponds, spider populations exhibited a dietary mixture of aquatic and terrestrial insects. These results indicate that both aquatic and terrestrial insects influence P. glacialis MeHg contamination. This suggests that all artic food webs, not just those connected to aquatic systems, may be contaminated with MeHg, suggesting that the Arctic is more contaminated than previously thought.

Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by cognitive decline and neuronal loss. Although amyloid-ß plaques and tau neurofibrillary tangles are well-established pathological hallmarks of AD, growing evidence suggests that additional mechanisms, including oxidative stress, iron dysregulation, and ferroptosis contribute significantly to the progression of the disease. Ferroptosis is an iron-mediated form of regulated cell death driven by lipid peroxidation and impaired antioxidant defenses. Neurons are particularly susceptible to ferroptotic damage due to their high metabolic demand, lipid-rich membranes, and reliance on highly regulated redox homeostasis. Disruption of the cystine/glutamate antiporter (system xc-) can deplete intracellular glutathione (GSH), impair glutathione peroxidase 4 (GPX4) activity, and promote the accumulation of toxic lipid peroxides, ultimately triggering ferroptotic cell death.

This study investigates the role of ferroptosis in oxidative neuronal injury using the immortalized HT-22 mouse hippocampal neuronal cell line, a well-established model of glutamate-induced oxytosis. Oxidative stress is induced through glutamate exposure, which inhibits cystine uptake via system xc- and depletes intracellular glutathione levels. Cell viability is assessed using MTT assays, and quantitative PCR is used to evaluate transcriptional changes in key genes involved in ferroptosis and antioxidant defense, including Nrf2, Slc7a11, Acsl4, Ptgs2, Sod2, and Catalase. To confirm the involvement of the ferroptotic pathway, the potent ferroptosis inhibitor Ferrostatin-1 (Fer-1) is employed to evaluate its ability to rescue neurons from glutamate-induced toxicity.

By characterizing both functional and transcriptional responses to oxidative stress, this research aims to better define the underlying molecular mechanisms by which glutamate toxicity leads to ferroptotic neuronal death. Understanding how ferroptosis contributes to neuronal vulnerability may reveal novel therapeutic targets aimed at strengthening antioxidant defenses and mitigating neurodegeneration in Alzheimer’s disease.

Alzheimer’s Disease (AD) is a neurodegenerative disease that is characterized by progressive neuronal death. AD can be identified by the presence of cytotoxic amyloid-ß plaque on neuronal synapses and misfolded tau tangles in the body of neurons. As the most common form of dementia, AD has become a hot topic for healthcare professionals, and researchers have looked for a better understanding of how to stop the progression of the disease. Recently, studies have looked into the antioxidant pathway as a target for controlling AD. Evidence shows that the presence of Aß-plaques and tau tangles generates oxidative stress in the form of reactive oxygen species (ROS). The persistence of ROS may lead to chronic inflammation and neuronal cell death. Our study looks at the effect of a novel drug, L2, on its ability to activate the antioxidant pathway in mouse cell models. The novel drug is designed to locate ROS and has antioxidant properties, and has been proven to reduce ROS in in vitro studies. If L2 is added into ROS-rich cell culture, then the antioxidant pathway will be activated and express the genes for antioxidant proteins. To test for activation of the antioxidant pathway, mouse microglial cells were treated with L2 and were lysed for messenger RNA (mRNA) extraction. Differentially expressed genes were quantified and analyzed using the RT-qPCR technique and RNA sequencing. Results of the data are still being analyzed.

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.