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.

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.

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.

“EVALUATING THE EFFECT OF NOVEL DRUGS ON LPS-INDUCED INFLAMMATION USING ENZYME-LINKED IMMUNOSORBENT ASSAY”

Neuroinflammation plays a key role in many neurodegenerative diseases and is characterized by the over-activation of immune cells within the central nervous system. Activated microglia and astrocytes release pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF- α), as well as reactive oxygen species that contribute to neuronal damage. These inflammatory responses are mediated through signaling pathways including the NF-κB pathway and the NLRP3 inflammasome.
Alzheimer’s disease (AD) is the most common neurodegenerative disease and the leading cause of dementia worldwide. In AD, accumulation of β-amyloid plaques (Aβ) stimulates chronic neuroinflammatory responses and contributes to neuronal dysfunction and disease progression. Elevated levels of inflammatory cytokines, particularly IL-1β, have been strongly associated with Aβ plaque deposition and the onset of AD.
Based on this relationship, targeting neuroinflammatory signaling pathways might be a promising therapeutic strategy for AD. PD2244, a novel compound synthesized by P2D Biosciences, is hypothesized to reduce neuroinflammation by suppressing the production of pro-inflammatory cytokines involved in AD pathology. Specifically, PD2244 is expected to decrease IL-1β production by inhibiting either the NF-κB pathway or the NLRP3 inflammasome.
To test this hypothesis, PD2244 was tested on several cells related to AD pathology, including microglial, neuronal, and monocytic. These cells were pretreated with increasing concentrations of PD2244 prior to inflammatory stimulation. IL-1β production was quantified using Enzyme Linked Immunosorbent Assay (ELISA), a highly sensitive technique commonly used to detect pro-inflammatory cytokine production.