Date of Completion

Summer 8-26-2022

Thesis Advisor(s)

David Knecht

Honors Major

Molecular and Cell Biology

Disciplines

Cell Biology

Abstract

Chemokinesis is the augmentation of cellular motility in response to chemical stimuli. While it is known that chemical factors induce changes in the behavior of a cell with regards to motility, the mechanism by which this process occurs is poorly understood. The aim of this project is to identify potential proteins within the signaling pathways that integrate the message brought on by chemical ligands and consequently lead to changes in cellular motility. In order to accomplish this goal, various gene knockout mutants of the amoeboid species Dictyostelium discoideum are compared to an axenic wild-type strain (AX2) based on their relative ability to demonstrate chemokinetic responses to the known chemokine folate. In wild-type strains of Dictyostelium discoideum, folate initiates an increase in cellular velocity (i.e. acceleration) as well as inducing positive chemotactic behavior within the amoeboid species. Therefore, the magnitude of acceleration when exposed to folate serves as a relative measurement of a cell’s ability to exhibit chemokinetic responses in the absence of a certain functional gene. These mutant strains are then compared to the wild-type strain AX2 to determine the extent to which the nonfunctional protein product of each mutant impedes the formulation of a chemokinetic response. As an additional comparison, chemical inhibitors that inhibit the same protein as several corresponding gene knockout mutants are utilized to see if there are any potential differences between the two routes of testing cellular chemokinesis.

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