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 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.

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.

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.

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.