Characterizing the role of Canoe as a cell junction-cytoskeletal linker protein during Drosophila morphogenesis
Public Deposited- Last Modified
- June 18, 2020
- Creator
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Ronk, Halle
- Affiliation: College of Arts and Sciences, Department of Biology
- Abstract
- Adherens junctions (AJs) connect epithelial cells to one another and connect the plasma membrane to the actomyosin cytoskeleton; this organization translates contractility to neighboring cells and preserves tissue integrity during morphogenesis. The exact interactions among adhesion molecules located at AJs remain unclear. It is currently thought that cadherins mediate cell-cell adhesion, while proteins bound to their cytoplasmic tails, known broadly as catenins, interact with junction-linker proteins. These linker proteins, in turn, interact with the actomyosin cytoskeleton. We examined whether Canoe acts as a junction-linker protein by testing its role in maintaining epithelial integrity, which is an indicator of junctional integrity. We used immunofluorescence and confocal microscopy to examine Drosophila melanogaster embryos during dorsal closure. In wild-type embryos, Canoe is enriched at the leading-edge epidermis and at multicellular junctions along the lateral epidermis. This enrichment pattern aligns closely with the location of actin filaments and myosin II heavy chain. We used RNA interference in conjunction with the UAS-Gal4 system to reduce canoe function. Loss of canoe caused cells along the lateral epidermis to become highly variable in shape, suggesting that translation of contractility to AJs occurred unevenly among the cell population. Furthermore, the number and regularity of puncta of Enabled, an actin assembly and elongation factor usually enriched at AJs, decreased along the leading edge. These results support the hypothesis that Canoe acts as a linker protein, playing an essential role in regulating epithelial sheet integrity and contractility. Understanding these complex interactions can provide insight into the mechanisms of wound healing and neural tube closure in humans and guide the creation of embryonic defect prevention therapies.
- Date of publication
- spring 2018
- Keyword
- DOI
- Resource type
- Rights statement
- In Copyright
- Note
- Funding: William W. and Ida W. Taylor Faculty-Mentored Research Fellowship, Summer 2017
- Funding: Honors Undergraduate Research Fund
- Advisor
- Peifer, Mark
- Degree
- Bachelor of Science
- Academic concentration
- Biology
- Honors level
- Honors
- Degree granting institution
- University of North Carolina at Chapel Hill
- Graduation year
- 2018
- Language
- English
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