Date of Completion

2016

Document Type

Honors College Thesis

Department

Biology

Thesis Type

College of Arts and Science Honors, Honors College

First Advisor

Alan Howe

Second Advisor

Bryan Ballif

Keywords

calcium, PKA, contractility, migration, actomyosin

Abstract

Cellular migration is a complex process that requires a cell to constantly sense extracellular stimuli and translate them into intracellular signaling responses. The act of migration requires an exertion of force by the cell via actomyosin contractile mechanisms to not only directionally pull the cell body, but also to maintain a tensional homeostasis with its environment. This “mechanoreciprocity” between the cell and the extracellular environment is regulated by a myriad of signaling pathways. Namely, calcium (Ca2+) and protein kinase A (PKA) have both been independently established as regulators of actomyosin contractility and cellular migration. Further, previous research has implicated calcium, PKA, and actomyosin contractility in a cyclic regulatory relationship that is vital to the regulation of migration and translation of extracellular stimuli into intracellular signaling. This study began the investigation into the signaling hierarchy of these factors by showing that an increase in intracellular calcium levels via uncaging results in an actomyosin dependent cellular contractile response, as well as a cell-wide increase in PKA activity. Additionally, this study provides enabling techniques for further investigation into the interplay between these factors by establishing a functional and replicable protocol for increasing intracellular calcium levels and visualizing cellular contractile forces.

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

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