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- Creators: School of Mathematical and Statistical Sciences
- Member of: Theses and Dissertations
- Status: Published
My work characterizes how two different classes of tools behave in new contexts and explores methods to improve their functionality: 1. CRISPR/Cas9 in human cells and 2. quorum sensing networks in Escherichia coli.
1. The genome-editing tool CRISPR/Cas9 has facilitated easily targeted, effective, high throughput genome editing. However, Cas9 is a bacterially derived protein and its behavior in the complex microenvironment of the eukaryotic nucleus is not well understood. Using transgenic human cell lines, I found that gene-silencing heterochromatin impacts Cas9’s ability to bind and cut DNA in a site-specific manner and I investigated ways to improve CRISPR/Cas9 function in heterochromatin.
2. Bacteria use quorum sensing to monitor population density and regulate group behaviors such as virulence, motility, and biofilm formation. Homoserine lactone (HSL) quorum sensing networks are of particular interest to synthetic biologists because they can function as “wires” to connect multiple genetic circuits. However, only four of these networks have been widely implemented in engineered systems. I selected ten quorum sensing networks based on their HSL production profiles and confirmed their functionality in E. coli, significantly expanding the quorum sensing toolset available to synthetic biologists.
In this project we focus on COVID-19 in a university setting. Arizona State University has a very large population on the Tempe Campus. With the emergence of diseases such as COVID-19, it is very important to track how such a disease spreads within that type of community. This is vital for containment measures and the safety of everyone involved. We found in the literature several epidemiology models that utilize differential equations for tracking a spread of a disease. However, our goal is to provide a granular look at how disease may spread through contact in a classroom. This thesis models a single ASU classroom and tracks the spread of a disease. It is important to note that our variables and declarations are not aligned with COVID-19 or any other specific disease but are chosen to exemplify the impact of some key parameters on the epidemic size. We found that a smaller transmissibility alongside a more spread-out classroom of agents resulted in fewer infections overall. There are many extensions to this model that are needed in order to take what we have demonstrated and align those ideas with COVID-19 and it’s spread at ASU. However, this model successfully demonstrates a spread of disease through single-classroom interaction, which is the key component for any university campus disease transmission model.