<p>A saugeye is the progeny of a female walleye (<i>Sander vitreus)</i> and male sauger (<i>Sander canadensis)</i>. In the United States, hybrid saugeyes are considered important for recreational fisheries and as a potential food source. Saugeyes grow exceptionally faster than their non-hybrid parents and are more tolerant of a broader range of water conditions. They are also of interest to anglers due to their increased growth rate and ease to catch. Rather unexpectedly, biologists have recently observed fish that they believe to be saugeye in the Fort Wayne Rivers even though only walleye have been stocked in the area. The fish in Hurshtown Reservoir are believed to be walleye and the identification of those in the Three Rivers is unknown. A potential source for saugeye in the Fort Wayne Rivers is St. Marys State Fish Hatchery in Ohio. This research aims to determine if the fish found in the Fort Wayne Rivers are walleye or saugeye using microsatellite analysis. Microsatellites at seven loci were genotyped for 20 reference walleye, sauger, and saugeye as well as 21 unknown fish caught near Fort Wayne. Of the fish caught near Fort Wayne, three are from Hurshtown Reservoir and 18 are from the Three Rivers. Assignment tests of genotypes were completed using model and non-model based cluster analysis. Genotypic variation clearly resolved the two parent species from their hybrid offspring. Sixteen of eighteen <i>Sander</i> (unknown species) caught in Fort Wayne Rivers between 2018 and 2019 were determined to be first generation saugeye. The other two were walleye found in the Maumee River downstream of Hosey Dam. The three <i>Sander</i> caught in Hurshtown Reservoir were verified to be walleye. Sauger have never been stocked in the Fort Wayne Rivers and connecting waterways. Therefore, it is not likely that the saugeye found in the analysis are from natural reproduction. It is speculated that saugeye are swimming to Fort Wayne from hatcheries within the Maumee watershed. There are many potential sources for walleye in the Fort Wayne Rivers. </p>

<p dir="ltr">Adipose tissue consists of adipocytes that store energy within lipid droplets and are a central component of lipid metabolism. Mammals contain white, brown and beige adipocytes, which differ in their metabolic roles. White adipocytes store energy, in the form of triglycerides, within lipid droplets and predominantly take on an energy storage role. Brown and beige adipocytes promote energy expenditure and the dissipation of energy as heat through non-shivering thermogenesis. Since energy expenditure combats excess caloric intake and overeating, non-shivering thermogenesis has become heavily researched for its potential therapeutic use in combatting the continued increase in obesity and metabolic disorders worldwide.</p><p dir="ltr">In addition to ATP synthesis, mitochondria are required for a multitude of metabolic processes that maintain cellular homeostasis, including non-shivering thermogenesis. Brown and beige adipocyte mitochondria are specialized to perform non-shivering thermogenesis in response to an environmental stressor like cold exposure. Uncoupling protein 1 (UCP1) is uniquely characteristic of brown and beige adipocyte mitochondria, because it allows oxidative phosphorylation to be uncoupled from ATP synthesis. In order to enhance non-shivering thermogenesis, ongoing molecular characterization of brown adipose tissue (BAT) is being conducted to identify proteins that regulate mitochondrial function and UCP1 activity. In this study, I explored the function of LETM1-domain containing 1 (LETMD1), a novel mitochondrial inner membrane protein with unknown function in BAT. We generated a global (<i>Letmd1</i>^<em>KO</em>) and UCP1+ cell-specific <i>(Letmd1</i>^<em>UKO</em><i>) knockout</i><i> </i>mouse model to study the whole-body and cell-autonomous role of LETMD1 in BAT, respectively. Loss-of-function studies resulted in striking, BAT-specific phenotypic differences, including whitened BAT under thermoneutral, room temperature and cold exposure. Both knockout models were cold intolerant without access to food, and became hypothermic within a few hours of fasted cold exposure. Loss of normal mitochondria structure and cristae arrangement were also evident in knockout BAT, resulting in a decreased number of mitochondria and decreased number of cristae per mitochondrion. Mitochondrial DNA copy number was also significantly decreased in both knockout models. Abnormal mitochondria morphology was supported by increased reactive oxygen species (ROS) accumulation in both knockout models and the visualization of protein aggregates and mitophagy-like morphologies in <i>Letmd1</i>^<em>UKO</em><i> </i><i>mice specifically</i>. TurboID proximity labeling of brown adipocytes revealed enrichment of several respiratory chain complex proteins, mitochondrial ribosome proteins and mitochondrial protein import machinery. Moreover, the aggregation of misfolded nuclear-encoded mitochondrial proteins, including several respiratory chain and mitochondrial ribosome proteins, suggested that LETMD1 facilitates mitochondrial protein import and mitochondrial ribosome assembly, thereby compromising respiratory chain assembly and function during non-shivering thermogenesis. Overall, this study identifies LETMD1 as a novel regulator of brown adipocyte mitochondrial structure and thermogenic function and highlights the requirement of LETMD1 for mitochondrial biogenesis.</p>

<p dir="ltr">Delta-like 1 (DLL1) is a protein on the surface of the cell that serves as a ligand for NOTCH receptors. Like NOTCH receptors, NOTCH ligands span the membrane of the cell and contain extracellular, transmembrane, and intracellular domains. NOTCH activation occurs through contact-dependent interactions between the NOTCH receptor on one cell and ligand on an adjacent cell. Previous studies have demonstrated that DLL1 predominantly functions cell non-autonomously to trigger NOTCH signaling in a neighbor cell but a cell-autonomous function of DLL1 has also been proposed in recent years. However, there is no direct evidence to support a cell-autonomous function of DLL1 in vivo. The overall goal of this thesis was to elucidate the cell-autonomous function of DLL1 by testing the hypothesis that the intracellular domain of DLL1 (DLL1ICD) can be cleaved and function in the DLL1-expressing cell in addition to triggering NOTCH signaling in a neighbor cell. The research strategy to test the hypothesis is by overexpression of full-length (FL) and cleaved Dll1 (Dll1ICD) in the murine myoblast cell line (C2C12). These plasmids utilize a tet-on system for inducible overexpression. Transfected myoblasts were used to analyze how overexpression of Dll1-FL and Dll1ICD affects proliferation, differentiation, fusion, and gene expression. The results show that Dll1-FL can be cleaved to generate an ICD. DLL1ICD overexpression promotes fusion without affecting proliferation. Further investigation reveals that overexpression of Dll1ICD affects the expression of NOTCH and myogenic-specific genes during differentiation, confirming the cell-autonomous role of DLL1ICD in myoblasts. These results together show that DLL1 can function cell autonomously through its intracellular domain to regulate myogenesis.</p>

<p dir="ltr">Across diverse organisms and tissues, aging cells undergo extensive rewiring on an epigenetic and transcriptomic level, leading to widespread changes in rhythmic gene expression. Rhythmic gene expression is dictated by the circadian rhythm, which is synchronized to the external environment through the detection of light by the eye. The photosensitive tissue of the eye, the retina, exhibits considerable age-dependent transcriptomic and epigenetic alterations. During aging, the prevalence of ocular disease increases along with a decline in visual function overall, predisposing older individuals to circadian rhythm desynchronization, which is associated with a host of pathologies including neurodegenerative disease and cancer. Despite links between the health of the eye during aging and circadian rhythm dysfunction, a cohesive understanding of the molecular underpinnings that tie these together has not been reached.</p><p dir="ltr">To first understand the transcriptional mechanisms that are necessary to maintain photoreceptor viability and function during aging, we performed a targeted photoreceptor-specific RNAi screen in <i>Drosophila </i>to identify transcriptional regulators necessary for protection against premature, age-dependent retinal degeneration. Using RNAi lines targeting transcription factors, chromatin remodelers, and histone modifiers, we identified 18 targets necessary for protection against premature and progressive retinal degeneration. These targets were enriched for factors involved in the regulation of RNA polymerase II (Pol II) initiation, pausing, and elongation, suggesting regulation of the transcription cycle is critical for photoreceptor health during aging. Transcriptome profiling of photoreceptors from select RNAi lines revealed that knockdown of the pausing factor <i>Spt5 </i>or the chromatin remodeler <i>domino </i>resulted in similar transcriptome-wide changes to those observed in aged photoreceptors. Together, these data showed that transcriptional regulators are key in maintaining photoreceptor viability during aging, and age-dependent changes in gene expression not only correlate with but may also contribute to an increased risk of retinal degeneration. This research is presented in Chapter 2: “Targeted RNAi screen identifies transcriptional mechanisms that prevent premature degeneration of adult photoreceptors”.</p><p dir="ltr">To determine how the chromatin landscape dictates changes in the photoreceptor transcriptome with aging, we profiled chromatin marks associated with active transcription in young and old <i>Drosophila </i>photoreceptors using ChIP-seq. Both H3K4me3 and H3K36me3 decrease globally across actively-expressed genes during aging independent of differential gene expression. Knockdown of the H3K36me3 methyltransferase Set2 in young photoreceptors led to substantial changes in splicing events similar to those observed in aging photoreceptors, impacting genes involved in phototransduction and neuronal function. Because proper splicing is essential for visual behavior, and <i>Drosophila </i>visual function decreases with age, H3K36me3 may play a role in maintaining visual function in the eye through the regulation of alternative splicing. This research is presented in Chapter 3: “Establishing the contribution of active histone methylation marks to the aging transcriptional landscape of Drosophila photoreceptors”.</p><p dir="ltr">Since the molecular circadian clock is necessary for light-dependent photoreceptor survival in <i>Drosophila</i>, we sought to characterize the rhythmic gene expression changes during aging by performing nuclear RNA-seq on young and old <i>Drosophila </i>photoreceptors across the circadian day. RNA-seq revealed that over 50% of the photoreceptor transcriptome is rhythmic, and one-third of expressed genes showed altered rhythmicity with age. CUT&RUN of the core molecular clock transcriptional activators CLOCK and CYCLE in young and old photoreceptors identified relatively few target genes, and that CLOCK and CYCLE occupancy on chromatin does not substantially change with age, suggesting other epigenetic factors underly the drastic shifts in the photoreceptor rhythmic transcriptome during aging. Profiling of H3K4me2/3, H3K36me3, H3K9me3, and H3K27me3 at a single time-point using CUT&RUN showed distinct patterns of distribution across genes in young and old photoreceptors, in addition to a genome-wide loss in levels of all marks. We performed ATAC-seq and CUT&RUN of Pol II, H3K4me1, H3K4me2, and H3K4me3 across the circadian day in young and old photoreceptors to observe their daily patterns. Chromatin accessibility and Pol II occupancy oscillate throughout the day at all expressed genes, and the phase of this oscillation shifts in old photoreceptors. This oscillating pattern occurred at all expressed genes regardless of the timing of rhythmic gene expression. H3K4me1, me2, and me3 showed different oscillating patterns at all expressed genes that were nearly abolished in old photoreceptors. Though the overall oscillating patterns of H3K4 methylation also did not correlate with the timing of rhythmic gene expression, levels of H3K4 methylation do correlate with when the gene is most highly expressed. CUT&RUN of H3K4 methylation in young photoreceptors with a knockdown of either of the H3K4 methyltransferases Trr or Trx determined that they have overlapping yet non-redundant roles in maintaining H3K4 methylation genome-wide. Transcriptome profiling of young photoreceptors with Trr or Trx knockdown showed that they are necessary for the majority of rhythmic gene expression in young photoreceptors. Additionally, Trr or Trx knockdown led to loss and modulation of rhythmic gene expression similar to the changes observed in aging photoreceptors. Together, these data suggest that the genome-wide decreases in histone methylation in aging photoreceptors are the driving force behind shaping the rhythmic transcriptome. This research is presented in Chapter 4: “Histone methylation loss underlies the rewiring of the rhythmic transcriptome in aging photoreceptors”.</p>

<p>The production of developmentally competent in vitro derived embryos is necessary to decreasing both economic and emotional losses. Epigenetic abnormalities/insults have been shown to occur at a higher incidence in in vitro embryos. An increased prevalence of epigenetic derived disorders such as Parkinson’s disease, Prader-Willi syndrome, and α-thalassemia as well as elevated preimplantation embryo arrest and reduced developmental rates are theorized to be caused by errors in the mediation of chromatin remodeling. Chromatin remodeling refers to the restructuring of packaged DNA so that transcription factors are either given more or less access to specific sequences. This can be done by covalent modification through histone methylation, acetylation, and phosphorylation as well as noncovalent modifications which employ ATP dependent chromatin remodeling complexes. The purpose of this thesis was to characterize two structurally integral core subunits, BAF155 and BAF170, of the SWI/SNF chromatin remodeling complex in porcine oocytes and preimplantation embryos. </p> <p>The first study concentrated on the transcript abundance of BAF155 and BAF170 in porcine oocytes and embryos. First, BAF155 and BAF170 transcript sequences were identified in porcine muscle and heart tissues. Those sequences were used to create quantitative polymerase chain reaction (qPCR) primers. mRNA from pools of GV oocytes (100-800) was converted to cDNA for transcript abundance measurements. However, transcript abundance remained too low for either BAF155 or BAF170 to be accurately quantified. </p> <p>The second study focused on developmental competency of embryos post interfering RNA (RNAi) knockdown of BAF155, BAF170, or both BAF155/BAF170 combined. After 7 days of culture, an analysis of variance (ANOVA) was performed to determine differences in mean nuclei numbers and morphological blastocyst percentages across the three groups. No significant difference was seen between means of treatment groups vs. both control groups. Significant differences were seen between siRNA and Non-Injected groups as well as Non-Injected and Scramble RNA groups. However this indicates that loss of BAF155, BAF170, or a combination of the two transcripts is not the driving force of the significant differences, rather the microinjection itself caused the differences.</p> <p>The third study examined the process by which BAF155 and BAF170 proteins are imported from the cytoplasm into the nucleus. It was hypothesized that karyopherin α 7 (KPNA7), a nuclear importer known to be prevalent in the porcine oocyte and early embryo, is the main importer of both subunits. A dominant-negative KPNA7 construct missing the importin beta binding (IBB) domain was microinjected into parthenogenetically activated embryos to outcompete competent wild-type KPNA7. No change in protein localization was seen at the 4-cell stage of development (48 hours post-injection) for either BAF155 or BAF170. To reinforce these results, an RNAi targeting KPNA7 was also microinjected into parthenogenetically activated embryos. Again, no change was shown in protein localization at the 4-cell stage (48 hours post-injection), indicating that KPNA7 was not the main nuclear importer of either BAF155 or BAF170.</p> <p>Further study is necessary to determine transcript abundance and the mechanism of nuclear import of both BAF155 and BAF170.</p><div><br></div>

<p>During gestation, the maternal liver undergoes various adaptive changes to cope with the increasing physiological and metabolic demands from both maternal and fetal compartments. Among these changes are robust growth and changes in transcriptome profile. However, how these events happen, and other aspects of this physiological phenomenon remains unexplored. Therefore, we aimed at further understanding how maternal liver responds to pregnancy. We used BrdU labeling combined with a virus-based tracing approach to quantify the percentage of maternal hepatocytes undergoing DNA synthesis and division over the course of gestation in mice. </p> <p>We found that ~50% maternal hepatocytes entered S-phase but, unexpectedly, did not undergo cytokinesis. This strongly suggests that maternal hepatocytes in fact undergo endoreplication instead of hyperplasia, as believed previously. Pericentral Axin2⁺ hepatocytes were reported to behave as liver stem cells responsible for liver homeostasis and turnover. We generated an <i>in vivo</i> fate-tracing mouse model to monitor the behavior of these cells in the maternal liver. Our results showed that they did not proliferate during pregnancy, homeostasis, and following partial hepatectomy. Curiously, we uncovered that, hepatocytes exhibit developmental phenotypes at mRNA level pre-pregnancy and at both mRNA and protein level during pregnancy. In the non-pregnant state, hepatocytes reserved mRNA expression of liver progenitor marker genes <i>Cd133</i> and <i>Afp</i>, which are localized in the nuclei, without protein translation. During gestation, maternal hepatocytes displayed cytoplasmic translocation of <i>Cd133</i> and <i>Afp</i> transcripts, concomitant with corresponding protein expression. </p> <p>Overall, all maternal hepatocytes became CD133⁺, and a subset of them express AFP. Additionally, in non-pregnant livers, mRNA of <i>Epcam</i>, another liver progenitor marker, was expressed within majority of hepatocytes, whereas its protein was solely translated in the pericentral region. In contrast, by end-gestation, EPCAM protein expression switched to the periportal region. These observations indicate that maternal hepatocytes exhibit heterogeneous developmental phenotypes, partially resembling fetal hepatocytes. It is intriguing why mature hepatocytes dedifferentiate into a progenitor state in response to pregnancy. AFP is considered to be produced primarily from fetal liver and thus is used to evaluate fetal development health. </p> A potential clinical relevance of our data is that we identified maternal liver as a new source of AFP. The hippo signaling pathway has been shown to potently control liver growth and hepatocyte heterogenicity. Surprisingly, we found that pregnancy neither altered the expression nor activities of the components of this pathway and its effector YAP1/TAZ. This finding indicates that pregnancy-induced maternal liver growth is not driven by hippo-YAP1 pathway. However, we demonstrate that the presence of YAP1 is essential for CD133 protein expression in maternal hepatocytes. Collectively, we revealed that, as pregnancy advances, maternal hepatocytes likely undergo endoreplication and display developmental phenotypes. Mechanistically, YAP1 dictates the expression of CD133, contributing to the pregnancy-dependent phenotypic changes of maternal hepatocytes.

<p>  </p> <p>Down syndrome (DS) is caused by the partial or complete trisomy of human chromosome 21 (Hsa21) and can result in skeletal deficits, including lower bone mineral density (BMD) and increased risk of fracture and osteoporosis or osteopenia earlier than the general population. Mouse models of DS have been developed to understand the genetic mechanisms resulting in these phenotypes, but models differ due to the complex genetic nature of DS and differing genome structures between humans and mice. Ts65Dn mice have been a popular model of DS as they contain ~50% of Hsa21 orthologous genes on a freely segregating minichromosome, but there is speculation that the phenotypes are exaggerated by non-Hsa21 orthologous trisomic genes also present. To address this issue, the Ts66Yah mouse model was developed to remove the non-Hsa21 orthologous trisomic genes. In this study, male and female Ts66Yah mouse femurs were evaluated during bone accrual and peak bone mass to investigate structural differences using micro-computed tomography. Additionally, the role of trisomic <em>Dyrk1a</em>, a Hsa21 gene previously linked to bone deficits in Ts65Dn mice, was evaluated through genetic and pharmacological means in Ts66Yah femurs at postnatal day 36. Ts66Yah mice were found to have little or no trabecular deficits at any age evaluated, but sex-dependent cortical deficits were present at all ages investigated. Reducing <em>Dyrk1a</em> copy number in Ts66Yah mice significantly improved cortical deficits but did not return cortical bone to euploid levels. Pharmacological treatment with DYRK1A inhibitor L21 was confounded by multiple variables, making it difficult to draw conclusions about DYRK1A inhibition in this manner. Overall, these results indicate trabecular deficits associated with Ts65Dn mice may be due to the non-Hsa21 orthologous trisomic genes, and more Hsa21 orthologous trisomic genes are necessary to produce trabecular deficits in DS model mice. As more mouse models of DS are developed, multiple models need to be assessed to accurately define DS-associated phenotypes and test potential treatments.</p>

The Keap1-Nrf2 pathway regulates a wide range of cytoprotective genes, and has been found to serve a protective and beneficial role in many body systems. There is limited information available, however, about its role in bone homeostasis. While Nrf2 activation has been suggested as an effective method of increasing bone mass and quality, there have been conflicting reports which associate Keap1 deficiency with detrimental phenotypes. As Keap1 deletion is a common method of Nrf2 activation, further study should address the impacts of various methods of regulating Nrf2 expression. Also, little research has been conducted on the specific pathways by which Nrf2 activation improves bone quality. In this study, the effects of alterations to Nrf2 activation levels were explored in two specific and varied scenarios. In the first experiment, moderate Nrf2 activation was achieved via partial deletion of its sequestering protein, Keap1, in an aging mouse model. The hypothesis tested here is that moderate Nrf2 activation improves bone quality by affecting bone metabolism and response to mechanical loading. The results of this first experiment suggest a subtle, sex-specific effect of moderate Nrf2 activation in aging mice which improves specific indices of bone quality to varying degrees, but does not affect loading-induced bone formation. It is likely that the overwhelming phenotypic impacts associated with aging or the systemic effects of global Keap1 deficiency may increase the difficulty in parsing out significant effects that can be attributed solely to Nrf2 activation. In the second experiment, a cell-specific knockout of Nrf2 in the osteocytes was achieved using a Cre/Lox breeding system. The hypothesis tested here is that osteocyte-specific deletion of Nrf2 impairs bone quality by affecting bone metabolism and response to mechanical loading. The results of this experiment suggest an important role of Nrf2 in osteocyte function which improves certain indices of bone quality, which impacts male and female bones in different 7 ways, but did not significantly impact loading-induced bone formation. Further studies should modify the method of Nrf2 activation in an effort to refine the animal model, allowing the effects of Nrf2 to be isolated from the potential systemic effects of Keap1 deletion. Future studies should also utilize other conditional knockout models to elucidate the effects of Nrf2 in other specific cell types.

<p>  G Protein Coupled Receptor (GPCR) signaling plays a key role in intercellular communication and regulates many physiological processes relevant to disease. Approximately 30-40% of all FDA approved drugs target GPCR pathways, but limitations and off-target side effects remain obstacles. Regulator of G protein Signaling (RGS) proteins negatively modulate GPCR signaling by accelerating deactivation of the Gα subunit and thus represent a novel alternative to current approaches. While research on RGS proteins and how they are regulated has expanded rapidly, there are still gaps in knowledge for some members of the RGS family. One example is RGS2, which is selective for Gαq signaling. Lowered RGS2 levels are implicated in numerous diseases, and while the E3 ligase responsible for facilitating degradation of RGS2 has been identified more work needs to be done to viably drug it to enhance RGS2 protein levels. In this thesis, I explore how FBXO44, an E3 ligase substrate recognition component responsible for RGS2 degradation, interacts with RGS2 to explore approaches to inhibit degradation.</p> <p><br></p> <p>While the FBXO44-RGS2 interaction has been demonstrated previously, the degron sequence of RGS2 remained unknown. We hypothesized that FBXO44 binds RGS2 at its Nterminus and investigated this using N-terminally truncated RGS2 constructs. Our results indicated that FBXO44 binds between residues 5 and 16 of RGS2, as removal of these stabilized RGS2 against proteasomal degradation. Based on these results we designed a peptide microarray to identify important residues and properties for FBXO44 in vitro and found that Cys13 is essential for FBXO44 binding.</p> <p><br></p> <p>We also developed and optimized a high-throughput split luciferase screen to identify potential inhibitors of the FBXO44-RGS2 interaction. After forming a cell-line stably expressing tagged FBXO44 and RGS2 and optimizing assay condition, we achieved a robust assay for screening as determined by Z’-factor. <br>  </p>

<p>Sea urchins are fascinating marine creatures belonging to the phylum Echinodermata that serve as an essential ecological component and hold promise as a prospective source of therapeutics. However, sudden environmental changes, such as global warming and marine pollution, are placing significant stress on these organisms. To maintain natural resources and exploit sea urchins commercially, researchers are investigating aquaculture as a solution.</p> <p>This investigation discloses the physiological and immunological effects of physical and chemical stressors on one of the most common edible species of sea urchin, <em>Arbacia punctulata</em>. The study employed an elevated temperature as a physical stressor (1°C/day), lipopolysaccharides (LPS) inoculation as a chemical stressor (4µg/ml/day), and a combination of both LPS and elevated temperature as combined stressors. The results demonstrated a significant alteration in the total and differential coelomocyte count in the LPS-stressed group (p<0.05) and combined stressed group (p<0.05) followed by abnormal behavioral activity compared to those of control. Additionally, exposure to acute LPS exposure (at day 1 and day 3) and combined stressors led to an increase in phagocytic capacity (p<0.05) and lysozyme activity (p<0.05). Chronic exposure to LPS and combined stressors resulted in a decrease in gonadosomatic index (p<0.05, at day 10) and lysozyme activity (at day 7). A significant increase in coelomic fluid (CF) protein (p<0.05)was observed in the temperature-stressed group on days 5 and 10, while the combined stressed group had significantly more CF protein on days 1, 5, 7, and 10. An upregulation of Nf-kB gene expression was also observed (p>0.05) in temperature stressed group.  </p> <p>The study also revealed that sea urchins contain bioactive compounds that protect against external and internal injury, cell death, and body wall extract of sea urchin exhibited high antioxidant activity(p<0.05). Furthermore, it confirmed the antibacterial activity (p<0.05) of sea urchin (<em>Arbacia punctulata </em>and<em> Lytechinus variegatus</em>) body wall and coelomic fluid (cell-free plasma) extracts against ten pathogenic bacteria. The ethyl acetate body wall extract of both sea urchin species demonstrated higher inhibitory activity against the pathogenic bacteria tested. Overall sea urchin has potentials to meet the demand of food and medicine. </p>