Document Type

Honors Thesis

Publication Date



As a ubiquitous intracellular messenger ion, calcium is involved in many critical biochemical processes in the cell. In cardiomyocytes, Ca2+ interacts with a variety of calcium-sensing proteins and regulates cardiac pacemaking, excitability and contractility. This study examined two typical calcium-sensing proteins: calpain and Ca2+/calmodul independent protein kinase II (CaMKII). Drosophila melanogaster was used as a model to explore the roles of these proteins in cardiomyocyte and how their dysregulation affects cardiac function. We show here that calpain mutations, calpain knockdowns, and CaMKII knockdown result in increased cardiac frequency and rhythmicity. In contrast, mutation in CaMKII causes a decreased cardiac frequency and rhythmicity. The findings deepened our understanding of the roles of calpain and CaMKII in heart cells and how their dysregulation could affect the heartbeat.

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