Matching Items (37)
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- All Subjects: Genetics
- Creators: School of Life Sciences
Description
The use of genetic management in conservation has sparked much debate around the ethical and environmental impacts of the plans. A case study on the conservation of leopard frogs in Arizona was analyzed to better understand the benefits and issues surrounding genetic management plans. The first part of the case focuses on the recent management plan for Chiricahua Leopard Frogs implemented by the Arizona Game and Fish Department. The goal of the plan is to better understand the genetic dynamics of the established Chiricahua Leopard Frog populations to develop a more effective management plan. The second part of the case focuses on the Arizona Game and Fish Department’s management of the Northern Leopard Frog. There was little success with the initial breed and release program of the native species, however a nonnative subspecies of Northern Leopard Frog was able to establish a thriving population. This case study exemplifies the many complications with genetic management plans and the importance of careful assessment of options when deciding on a genetic management plan. Despite the complexity of genetic management plans, it is an important method to consider when discussing the conservation of a species.
ContributorsTurpen, Alexa (Author) / Murphree, Julie (Thesis director) / Collins, James (Thesis director) / Owens, Audrey (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor) / College of Integrative Sciences and Arts (Contributor) / School of Mathematical and Natural Sciences (Contributor)
Created2024-05
Description
Tissue regeneration is a complex process that activates both developmental and metabolic signaling pathways (Kashio & Miura, 2020). The wing imaginal disc in Drosophila melanogaster has been invaluable in discerning what pathways are activated during tissue regeneration, which is typically done by genetically or physically wounding the wing disc and using fluorescent markers to track different signals. However, despite its importance in other regeneration contexts (Tafesh-Edwards & Eleftherianos, 2020), immune signaling has not been well studied in this tissue. Furthermore, what we do know about tissue regeneration and immune signaling is specific to apoptotic cellular death, less is known about other types of cellular death, such as necrotic cellular death and the consequent signaling systems that result from necrosis. Drosophila have an open immune system and only possess innate immunity (Pastor-Pareja et al., 2008), making them an ideal model to study hemocyte involvement in tissue regeneration. Hemocytes are equivalent to blood cells in vertebrates, and are involved in immunological response (Kurucz et al., 2003). In this work, we observed hemocyte accumulation during injury-induced regeneration. Cellular damage was induced using a genetic ablation system known as DUAL Control, with hemipterous CA and GluR1 used to induce apoptotic and necrotic cell death respectfully. We have discovered that while hemocytes are recruited to the wing disc upon both apoptotic and necrotic injury, necrotic tissue has more hemocytes adhered than apoptotic tissue. The difference in adherence could be due to basement membrane integrity being damaged more severely in necrotic discs than apoptotic discs. Our results show that hemocytes are attracted to wing discs that have undergone necrotic damage, indicating that the immune system plays some sort of role in necrotic cellular death. Though the immune response to different types of tissue damage in Drosophila is much simpler than in vertebrate models, there are many similarities between the two, and could lead to research involving human immune signaling as it pertains to regeneration.
ContributorsZustra, Ayla (Author) / Harris, Robin (Thesis director) / Gile, Gillian (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2022-05
Description
Most protein-coding mRNAs in eukaryotes must undergo a series of processing steps so they can be exported from the nucleus and translated into protein. Cleavage and polyadenylation are vital steps in this maturation process. Improper cleavage and polyadenylation results in variation in the 3′ UTR length of genes, which is a hallmark of various human diseases. Previous data have shown that the majority of 3’UTRs of mRNAs from the nematode Caenorhabditis elegans terminate at an adenosine nucleotide, and that mutating this adenosine disrupts the cleavage reaction. It is unclear if the adenosine is included in the mature mRNA transcript or if it is cleaved off. To address this question, we are developing a novel method called the Terminal Adenosine Methylation (TAM) assay which will allow us to precisely define whether the cleavage reaction takes place upstream or downstream of this terminal adenosine. The TAM Assay utilizes the ability of the methyltransferase domain (MTD) of the human methyltransferase METTL16 to methylate the terminal adenosine of a test mRNA transcript prior to the cleavage reaction in vivo. The presence or absence of methylation at the terminal adenosine will then be identified using direct RNA sequencing. This project focuses on 1) preparing the chimeric construct that positions the MTD on the mRNA cleavage site of a test mRNA transcript, and 2) testing the functionality of this construct in vitro and developing a transgenic C. elegans strain expressing it. The TAM assay has the potential to be a valuable tool for elucidating the role of the terminal adenosine in cleavage and polyadenylation.
ContributorsKeane, Sara (Author) / Mangone, Marco (Thesis director) / Lapinaite, Audrone (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor) / Department of English (Contributor)
Created2023-05
Description
Hepatocellular carcinoma (HCC) is the most common type of liver cancer and has been shown to have genetic factors that contribute to cancer susceptibility. These genetic factors can be studied using Genome-Wide association studies (GWAS), which allow for the assessment of associations between specific biologic markers. Through GWAS, associations can be analyzed to identify genetic components that contribute to the onset of HCC. This study uses an extended version of Pathways of Distinction analysis (PoDA) to identify the subset of SNPs within the Antigen Presentation and Processing Pathway that distinguish cases from controls. Further analysis was performed to explore SNP-SNP association differences between HCC cases and controls using R-squared values and p-values. Three SNPs show significant inter-SNP associations in both HCC cases and controls. Additionally, 4 SNPs showed significant SNP-SNP associations exclusively in the control data set, possibly suggesting that control pathways have a greater degree of genetic regulation and robustness that is lost in carcinogenesis. This result suggests that these SNP associations may contribute to HCC susceptibility.
ContributorsAghili, Ardesher Joshua (Author) / Buetow, Kenneth (Thesis director) / Wilson Sayres, Melissa (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2016-05
Description
Schizophrenia affects 1.1% of the population worldwide. Schizophrenia is a complex, multifactorial disorder. Stress can trigger psychotic episodes and exacerbate schizophrenic symptoms. For humans, one gene implicated in stress and schizophrenia in humans is the early growth response 3 (EGR3). Patients with genomic variations in EGR3 have reduced levels of EGR3 in the prefrontal brain region compared with healthy patients. Schizophrenic patients also have less serotonin 2A receptor (5HT2AR), which is coded by the gene Htr2a, in their prefrontal cortex. Mice that are Egr3-deficient also have decreased levels of 5HT2AR, suggesting that Egr3 may be involved in the regulation of 5HT2AR. The purpose of the experiment is to determine if EGR3 binds to the Htr2a gene promoter region by using a Chromatin immunoprecipitation (ChIP) assay. We will use ECS to increase EGR3 expression. Previously we have identified two upstream sites of interest where EGR3 potentially binds to the Htr2a gene, one which is distal and one proximal to the transcription start site. After ECS, increased binding is seen in the Htr2a distal region with EGR3 via the ChIP assay. Increased binding was not observed at either of the promoter sites; however, the t-test comparing the distal site of the ECS and the No ECS groups to have a p-value of 0.056, suggesting that increasing the number of animals (n=7) could possibly give a more accurate representation to test our hypothesis. However, the experiment still suggests increased expression and that EGR3 may bind to the distal site of Htr2a. Keywords: stress, environment, genetics, schizophrenia, EGR3, chromatin immunoprecipitation
ContributorsMishra, Abhinav (Author) / Buetow, Kenneth (Thesis director) / Gallitano, Amelia (Committee member) / Zhao, Xiuli (Committee member) / Barrett, The Honors College (Contributor) / School of Politics and Global Studies (Contributor) / School of Life Sciences (Contributor)
Created2015-05
Description
Cancer is a disease in which abnormal cells divide uncontrollably and destroy body tissue, and currently plagues today’s world. Carcinomas are cancers derived from epithelial cells and include breast and prostate cancer. Breast cancer is a type of carcinoma that forms in breast tissue cells. The tumor cells can be further categorized after testing the cells for the presence of certain molecules. Hormone receptor positive breast cancer includes the tumor cells with receptors that respond to the steroid hormones, estrogen and progesterone, or the peptide hormone, HER2. These forms of cancer respond well to chemotherapy and endocrine therapy. On the other hand, triple negative breast cancer (TNBC) is characterized by the lack of hormone receptor expression and tends to have a worse prognosis in women. Prostate cancer forms in the cells of the prostate gland and has been attributed to mutations in androgen receptor ligand specificity. In a subset of triple negative breast cancer, genetic expression profiling has found a luminal androgen receptor that is dependent on androgen signaling. TNBC has also been found to respond well to enzalutamide, a an androgen receptor inhibitor. As the gene of the androgen receptor, AR, is located on the X chromosome and expressed in a variety of tissues, the responsiveness of TNBC to androgen receptor inhibition could be due to the differential usage of isoforms - different gene mRNA transcripts that produce different proteins. Thus, this study analyzed differential gene expression and differential isoform usage between TNBC cancers – that do and do not express the androgen receptor – and prostate cancer in order to better understand the underlying mechanism behind the effectiveness of androgen receptor inhibition in TNBC. Through the analysis of differential gene expression between the TNBC AR+ and AR- conditions, it was found that seven genes are significantly differentially expressed between the two types of tissues. Genes of significance are AR and EN1, which was found to be a potential prognostic marker in a subtype of TNBC. While some genes are differentially expressed between the TNBC AR+ and AR- tissues, the differences in isoform expression between the two tissues do not reflect the difference in gene expression. We discovered 11 genes that exhibited significant isoform switching between AR+ and AR- TNBC and have been found to contribute to cancer characteristics. The genes CLIC1 and RGS5 have been found to help the rapid, uncontrolled growth of cancer cells. HSD11B2, IRAK1, and COL1Al have been found to contribute to general cancer characteristics and metastasis in breast cancer. PSMA7 has been found to play a role in androgen receptor activation. Finally, SIDT1 and GLYATL1 are both associated with breast and prostate cancers. Overall, through the analysis of differential isoform usage between AR+ and AR- samples, we uncovered differences that were not detected by a gene level differential expression analysis. Thus, future work will focus on analyzing differential gene and isoform expression across all types of breast cancer and prostate cancer to better understand the responsiveness of TNBC to androgen receptor inhibition.
ContributorsDeshpande, Anagha J (Author) / Wilson-Sayres, Melissa (Thesis director) / Buetow, Kenneth (Committee member) / Natri, Heini (Committee member) / School of Human Evolution & Social Change (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2019-05
Description
Background: Dyslexia is a neurodevelopmental impacting reading and writing ability present in around 5 to 9 percent of the population. The etiology of the condition is not currently well understood.
Purpose: To identify new genes of interest regarding the etiology of dyslexia, describe the interaction of those genes within known gene networks, and discuss potential relationships between their expression in the early developing brain and phenotypic outcomes.
Method: With informed consent, participants’ phenotypic and exome data were collected. Phenotypic data were collected using assessments measuring reading and spelling ability. Exome data were collected via saliva samples and processed at the UW-CRDR. Exome data were then filtering using Seqr and compared across participant families. Certain genes with identical variations were visually validated using the Integrated Genome Viewer, and then investigated using STRING Network Analysis and the Human Brain Transcriptome.
Results: Three genes were identified: BCL6, DNAH1, and DNAH12. Protein-protein interactions were confirmed between DNAH1 and DNAH12 via STRING Network Analysis. BLC6 and DNAH1 experience higher postnatal expression in the cerebellar cortex. DNAH12 experiences higher prenatal expression in the hippocampus.
Discussion: The findings appear to be consistent with a heterogenous and polygenic model of dyslexia. The correlation between the participants’ genotypes and phenotypes is not strong enough to draw significant conclusions regarding genotype/phenotype connections. A larger participant sample size and analysis of a large pool of shared genes may reveal a clearer relationship.
ContributorsBanta, Claire (Author) / Peter, Beate (Thesis director) / Liu, Li (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor) / Sanford School of Social and Family Dynamics (Contributor) / College of Integrative Sciences and Arts (Contributor)
Created2024-05