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.