Researcher(s)
- Heather Boliver, Biological Sciences, University of Delaware
Faculty Mentor(s)
- Sadia Islam, , University of Delaware
Abstract
The ocular lens is composed of two types of cells: epithelial cells and fiber cells. Throughout our entire lifetime, the lens epithelial cells at the equator go through remarkable physical transformations as they differentiate (transform) into fiber cells. This process of cell shape changes is crucial for the lens growth, development and aging. However, little is known about the process that regulates lens epithelial cell shape changes before transforming into fiber cells. We have previously shown that non-muscle myosin IIA (NMIIA; Myh9), an actin-binding motor protein, regulates epithelial cell shape changes and packing during lens fiber cell differentiation. Loss of normal NMIIA function due to E1841K mutation causes irregular cell shape and impairs proper cell-to-cell contact. As proper cell-cell contact depends on recruitment of cell-cell adhesion proteins to “stick” the cells together, we hypothesize that NMIIA-E1841K mutation disrupts cell-cell adhesion proteins expression and/or localization that are required to maintain proper cell-cell contact during epithelial cell shape changes. To test this hypothesis, we have used western blots to verify the presence of important cell-cell adhesion complex components such as E-Cadherin, Vinculin, α-Catenin, and β-catenin. We have also performed immunofluorescence staining on immortalized mouse lens epithelial cell (imLEC) lines to investigate the presence of these adhesion complex proteins at cell-cell contact sites. Our western blot analysis and immunofluorescence staining confirm the presence of these cell-cell adhesion proteins in control lens epithelial cells and imLECs. Further analysis is required to compare the protein levels and localization of cell-cell adhesion proteins in control vs NMIIA-E18941K mutant lens epithelial cells.