Nucleolar Protein 56 is required to assemble the 60S subunit of ribosomes and is crucial for translating mRNA to protein. This study was conducted to uncover the functional identity and to clone the Nucleolar Protein 56 gene from Strongylocentrotus purpuratus. The BLAST, EchinoBase, and Interpro databases were utilized to analyze the Nucleolar Protein 56 gene’s identity based on its sequence and a subsequent phylogenetic tree was generated to further confirm the identity of the gene. PCR was used to amplify the gene followed by column purification. Nucleolar Protein 56 was introduced into a plasmid through a ligation experiment followed by transformation in competent bacteria. To analyze whether cloning was successful, colony PCR gel electrophoresis and a restriction digest were conducted. The analysis, however, revealed inconclusive results which may have been due to too little template DNA for the Colony PCR. The findings from this project can be applied to human patients with Spinocerebellar ataxia type 36 as it is caused by mutations in the Nucleolar Protein 56 genetic sequence in the cerebellum neurons.

Congenital heart diseases remain a leading cause of birth defect-related mortality, affecting nearly 1% of newborns worldwide. While genetic factors have dominated research attention, understanding of physical mechanisms governing cardiac development remains incomplete. This study explores how biomechanical forces and tissue deformation patterns influence heart morphogenesis. The research examines how tissue-level deformation dynamics contribute to cardiac development and how alterations might cause congenital defects. A novel imaging framework was developed using lineage-traced cell pairs in mouse models. The methodology combines Mosaic Analysis with Double Markers with aMHC-Cre expression to fluorescently label daughter cell pairs. Using light-sheet microscopy and computational analysis, the approach quantifies local tissue deformation across the developing heart. The analytical framework was verified through the successful visualization of cardiomyocyte pairs throughout E18.5 hearts. Preliminary results suggest that cell displacement is strongly biased to local fiber orientation. This leads to anisotropic tissue deformation that contributes to proper heart development. This research bridges developmental biology with biomechanics, offering insights into the physical basis of congenital heart defects. By identifying how coordinated tissue extension patterns are disrupted in disease models, this work establishes a novel framework for understanding cardiac developmental disorders and identifying potential therapeutic targets

Reproductive aging has profound effects on women, affecting not only fertility but other aspects of their overall health. As hormones produced in the ovaries often act as regulators of downstream organ systems and processes, ovary function and its progressive decline are a significant topic in improving health outcomes in women. Unlike many other mammals, bats seemingly do not exhibit the characteristic decline in reproductive health associated with ovarian aging. This project aims to investigate age-related changes in ovarian follicular populations between adult and geriatric Glossophaga soricina using histological analysis of ovarian tissue samples. Samples were analyzed for quantification of follicle numbers, types, and densities to examine if preservation of follicular structures in the geriatric age group can explain their extended reproductive lifespan. These findings will contribute to the characterization of follicular atresia rates and patterns unique to this long-lived bat species. Additionally, there is opportunity to discover morphological adaptations in the ovarian vasculature that support extended reproductive function. Overall, this project has the potential to identify evolutionary adaptations that allow maintenance of follicular reserves despite advanced aged.

There are a dozen established hallmarks of aging; however, much remains unclear regarding the interplay between them. The host lab is interested in investigating the relation between mitochondrial dysfunction and chronic inflammation or “inflammaging.” Elevated permeabilization of dysfunctional mitochondria has been found to allow leakage of mitochondrial DNA (mtDNA) into the cytosol, which can trigger inflammatory responses due to their prokaryotic origin. The host lab has demonstrated that mtDNA accumulates in the cytosol of aged flies and that preventing this accumulation ameliorates the immune response activation associated to aged organisms. Thus, manipulating mechanisms involving removal and recognition of cytosolic DNA may improve organismal health and lifespan. For example, DNase II, a lysosomal nuclease, and Stress Induced DNase (SID), an immune response nuclease, are of interest due to their ability to degrade cytosolic DNA. In relation, Eyes absent (Eya), a transcription factor that regulates eye development, is responsible for activating the immune pathway in the presence of endogenous dsDNA. I will employ the use of Drosophila melanogaster’s drug-inducible systems to induce temporal and tissue specific expression of the aforementioned genes that can regulate mtDNA. The aim of this project is to understand the significance of glia in regards to mtDNA accumulation, inflammation, and overall organismal health given their established role in age-related neurodegeneration.

The trabecular meshwork (TM) is the primary site of aqueous humor outflow in the eye and plays a crucial role in maintaining intraocular pressure (IOP). Dysfunction of the TM can lead to elevated IOP, a key risk factor in the development of glaucoma. Previous studies have identified mitochondrial damage in glaucomatous TM cells. To model this pathology, we treated primary human TM cells with ammonium (NH₄), mimicking conditions observed in glaucomatous cells. Using an extracellular flux assay on a Seahorse XF Analyzer 96-well microplate, we analyzed the metabolic profile of NH₄-treated TM cells, focusing on parameters such as spare respiratory capacity, ATP production rate, oxygen consumption rate (OCR), and extracellular acidification rate (ECAR). This analysis provided detailed insight into mitochondrial function, including basal respiration, ATP-linked respiration, proton leak, maximal respiration, spare respiratory capacity, and non-mitochondrial respiration. These data will help determine whether NH₄ treatment induces upregulated mitochondrial activity in TM cells. Such metabolic shifts may be linked to increased reactive oxygen species (ROS) production, potentially contributing to TM dysfunction and increased aqueous humor outflow resistance, a hallmark of glaucomatous pathology. Further assays can be conducted to directly assess ROS involvement in this process.