Date of Award

5-12-2023

Document Type

Thesis

Degree Name

Bachelor of Arts

Department

Biology

First Advisor

Wade Powell

Abstract

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates toxicity of dioxin-like compounds. In the absence of xenobiotics, AHR also plays roles in development and physiology, including promoting cell cycle progression through the G1/S checkpoint. Unlike humans and rodents, the frog Xenopus laevis expresses two paralogous AHR proteins, AHR1α and AHR1β, the result of a genome duplication approximately 17-18 million years ago. We recently generated mutant derivatives of the XLK-WG cell line lacking a functional version of either AHR1α or AHR1β. Growth of each strain was measured using colony formation assays and the water-soluble tetrazolium (WST-8) method, each demonstrating that AHR1α-/- cells proliferate approximately 30% more slowly than wild-type or the AHR1β-/- line. To investigate a potential mechanism underlying the slow growth phenotype, cell cycle distribution of each line was determined by propidium iodide staining and flow cytometry. AHR1β-/- cells and wild-type lines exhibited similar distributions of cells in the various stages. In contrast, AHR1α-/- cells exhibited a unique sub-G1 population. This indicates breakdown of genomic DNA and suggests that this mutant line has a heightened propensity for apoptosis. We tested this hypothesis directly using two approaches: Annexin V staining with flow cytometry for fixed cells and a caspase-3/7 assay in live cells. Neither approach detected increased apoptosis in AHR1α-/- cells. We next tested the hypothesis that AHR1α-/- cells in the sub-G1 population undergo pyroptosis, a distinct pathway of programmed cell death that resembles apoptosis in the breakdown of genomic DNA. A luminescent caspase-1 inflammasome assay revealed no increased pyroptosis, even in wild-type cells treated with talabostat, resiquimod, or PAM3CSK4, inducers of the pyroptosis pathway. We tentatively conclude that the slow growth and apparent degradation of genomic DNA in AHR1α-/- mutants occurs by a unique mechanism, as yet undetermined.

Rights Statement

All rights reserved. This copy is provided to the Kenyon Community solely for individual academic use. For any other use, please contact the copyright holder for permission.

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