04/06/2026
Biology and Neuroscience Seminars are open to the public and take place in Drew Science room 118 on Friday afternoons from 1:50 to 3:00. This week's seminar features students presenting their senior projects:
Malik Wynn ‘26 "Upper Forelimb Tricep Comparison: Cats and Fetal Pigs"
ABSTRACT: Forelimb anatomy in mammals reflects the mechanical demands of their ecological roles. Digging species often develop robust triceps and an extended olecranon process to generate powerful elbow extension, while running species favor longer distal limbs and reduced triceps mass to enhance speed and stride efficiency. This project investigates whether these ecological differences are mirrored in the forelimb musculature of domestic cats (Felis catus) and fetal pigs (Sus domesticus), representing a runner and a rooter, respectively. The hypothesis was that pigs would exhibit proportionally larger triceps due to their rooting behavior which requires strong forelimb extension. To test this, dissections were performed on eight cats and eight fetal pigs. All three triceps heads were isolated and weighed, and the remaining upper forearm musculature was measured. A triceps-to-total–forelimb mass ratio was calculated for each specimen, and a Mann–Whitney U test was used to assess differences between species. Contrary to expectations, the results showed no significant difference in triceps proportion between cats and fetal pigs (U = 40, p = 0.44). One likely explanation is developmental stage: fetal pigs have not yet engaged in rooting behavior, and muscle growth is influenced by use and activity. These findings suggest that ecological function may not be reflected in forelimb musculature until later developmental stages. Future research should compare animals at matched stages of development and consider environmental factors such as housing and activity level to better understand how behavior shapes musculoskeletal anatomy.
Jessica Vo ‘26 "Investigating the neurodevelopmental effects of PFAS mixtures in a chicken embryo model"
ABSTRACT: Per- and polyfluoroalkyl substances (PFAS) are groups of synthetic compounds widely used in industrial and consumer products. Their strong carbon-fluorine bonds make them extremely resistant to breaking down, leading to environmental persistence, bioaccumulation, and both human and environmental health risks. Research has shown that early life exposure to PFAS compounds in humans can affect growth and development. While this is compelling, these studies have primarily been done in individual compounds, rather than PFAS mixtures, even though organisms are almost always exposed to these toxicants in combination. We hypothesized that exposure to these PFAS mixtures would cause dose-dependent increases in neural crest cell (NCC) death and significant alterations in mitochondrial density. This study investigates the developmental effects of PFAS mixtures on chicken embryos, a model system with early developmental processes that are comparable to those of humans. Mixtures of five compounds (PFOA, PFOS, PFBA, PFBS, or PFHxS) were injected into fertilized eggs at an environmentally relevant range of concentrations, ranging from 100nM to 100μM. Embryos were then dissected and neural tube sections explanted. NCCs were analyzed the following day using fluorescence microscopy to quantify cell death and mitochondrial quantity. Cell health was evaluated using Sytox Green live/dead staining, MitoTracker fluorescent dye was used for labeling for mitochondrial density, and NucBlue for visualizing the nuclei. Early results indicate that higher PFAS doses result in changes in development, reduced cell survival, and changes in mitochondrial abundance and quantity, with these effects increasing with the dose. Findings suggest that even low PFAS mixture exposures can negatively affect development. This research adds to the growing evidence that realistic, everyday levels of PFAS exposure may be harmful, highlighting the need for stronger policies that address PFAS mixtures rather than individual compounds.
Emmanuel Wachaga ‘26 "TBA"
ABSTRACT: Replicative immortality is a defining hallmark of cancer, primarily driven by activation of telomerase through upregulation of the telomerase reverse transcriptase (TERT) gene. In colorectal cancer, elevated TERT expression supports sustained proliferation, tumor progression, and resistance to apoptosis. Despite its central role, current approaches to inhibit telomerase are often transient and insufficient for long-term therapeutic benefit. Therefore, there is a critical need for strategies that achieve durable suppression of TERT activity. This proposal aims to test the hypothesis that CRISPR/Cas9-mediated disruption of the TERT promoter will result in sustained reduction of telomerase activity and impaired cancer cell survival. To address this, guide RNAs targeting regulatory regions of the TERT promoter will be designed using bioinformatics tools to maximize specificity. CRISPR/Cas9 will be introduced into colorectal cancer cells, and successful editing will be validated through sequencing. TERT expression will be quantified using RT-qPCR, while protein levels and DNA damage responses will be assessed via Western blotting. Telomerase activity will be measured using the TRAP assay. Functional outcomes, including cell proliferation and apoptosis, will be evaluated using proliferation assays and flow cytometry. Finally, the impact of TERT disruption on tumor growth will be assessed using an in vivo xenograft mouse model. It is anticipated that CRISPR-mediated targeting of the TERT promoter will reduce TERT expression, decrease telomerase activity, increase DNA damage signaling, and ultimately limit tumor growth. This study has the potential to establish a foundation for durable, gene-targeted cancer therapies.
