Presentation Type
Poster
Faculty Mentor’s Full Name
Beverly Piggott
Faculty Mentor’s Department
Department of Biological Sciences
Abstract / Artist's Statement
Calcium signaling is vital for the development of the nervous system. Calcium acts as an essential second messenger under the control of regulatory mechanisms such as calcium stores, membrane channels, pumps, and intracellular calcium-binding proteins. Its signaling pathways mediate stem cell division, differentiation, and identity. Calcium homeostatic disruptions are linked to neurodevelopmental disorders from hypocalcemia and autism spectrum disorder to schizophrenia. Calcium regulation is widely studied regarding its impact on cell signaling and function, but little is known about its effects on cell fate in neural progenitor cells. Neural progenitor cells give rise to the entire nervous system, and defects in their proliferation and differentiation have been linked to deficits in neonatal development and eventual cognitive dysfunction (Martina). Previous work in our lab found that reduced Sarcoendoplasmic Reticulum Calcium ATPase (SERCA) expression disrupted calcium levels, changed neural stem cell identity, and affected proliferation. To fully explore the role of calcium homeostasis in neural development, I manipulated the expression of calcium-binding protein, Calmodulin (CaM), and the sodium-calcium exchange channel (NCX). Downregulating cam and ncx may interfere with the controlled regulation of calcium in neural development. Downregulating calcium-signaling regulators with RNAi will contribute to a better understanding of the role of calcium-signaling regulators in stem cell identity and proliferation. Analyzing cell type-specific markers will reveal the calcium’s role in cell identity. By measuring stem cell size, count, and mitotic markers, I propose to identify cam and ncx will contribute to the growth and division of type II neural stem cell lineages in Drosophila Melanogaster. By better understanding the cooperative regulation of calcium and its significance to stem cell development, future research can pinpoint genetic regulators of calcium signaling molecules to treat mutations caused by calcium dysregulation in neural progenitor cells. This analysis of neural progenitor cells may provide insight into neurodevelopmental deficits. The better we understand neurodevelopment, the better the onset of these diseases can be identified, and the prognosis and treatment improved.
Category
Life Sciences
The Role of Calcium in the Neural Stem Cell Development
UC South Ballroom
Calcium signaling is vital for the development of the nervous system. Calcium acts as an essential second messenger under the control of regulatory mechanisms such as calcium stores, membrane channels, pumps, and intracellular calcium-binding proteins. Its signaling pathways mediate stem cell division, differentiation, and identity. Calcium homeostatic disruptions are linked to neurodevelopmental disorders from hypocalcemia and autism spectrum disorder to schizophrenia. Calcium regulation is widely studied regarding its impact on cell signaling and function, but little is known about its effects on cell fate in neural progenitor cells. Neural progenitor cells give rise to the entire nervous system, and defects in their proliferation and differentiation have been linked to deficits in neonatal development and eventual cognitive dysfunction (Martina). Previous work in our lab found that reduced Sarcoendoplasmic Reticulum Calcium ATPase (SERCA) expression disrupted calcium levels, changed neural stem cell identity, and affected proliferation. To fully explore the role of calcium homeostasis in neural development, I manipulated the expression of calcium-binding protein, Calmodulin (CaM), and the sodium-calcium exchange channel (NCX). Downregulating cam and ncx may interfere with the controlled regulation of calcium in neural development. Downregulating calcium-signaling regulators with RNAi will contribute to a better understanding of the role of calcium-signaling regulators in stem cell identity and proliferation. Analyzing cell type-specific markers will reveal the calcium’s role in cell identity. By measuring stem cell size, count, and mitotic markers, I propose to identify cam and ncx will contribute to the growth and division of type II neural stem cell lineages in Drosophila Melanogaster. By better understanding the cooperative regulation of calcium and its significance to stem cell development, future research can pinpoint genetic regulators of calcium signaling molecules to treat mutations caused by calcium dysregulation in neural progenitor cells. This analysis of neural progenitor cells may provide insight into neurodevelopmental deficits. The better we understand neurodevelopment, the better the onset of these diseases can be identified, and the prognosis and treatment improved.