Dejiah Julien, “Understanding the Role of Laminin-111 in Mediating Tissue Stress during MHB Morphogenesis in Zebrafish”
Mentor: Jennifer Gutzman, Biological Sciences, Letters & Science (College of)
Poster #14
Our research focuses on the study of brain morphogenesis to understand the mechanisms underlying structural birth defects during development. These defects are known to affect the structure of the brain long before birth, often resulting in neurological damage ranging from mild to severe cases. It has been established that brain development is controlled by many molecular and biomechanical factors, some of which mediate tissue folding. To identify the mechanisms that mediate brain morphogenesis, we are using the zebrafish embryonic model. Our work examines the highly conserved tissue fold that forms the midbrain-hindbrain boundary (MHB), the first fold in the vertebrate brain. In zebrafish we have identified the basement membrane protein laminin-111 as critical in mediating basal tissue folding during MHB morphogenesis. Current work in our lab has shown that laminin-111 mutants have higher tissue stress in their MHB during morphogenesis compared to wild-type embryos. We hypothesize that the number of cells within the MHB region may contribute to this increased stress. To test this hypothesis, we co-injected embryos with membrane-GFP and H2B-RFP mRNA to label cell membranes and nuclei, so we can count the number of epithelial cells in the MHB region in wildtype zebrafish versus laminin-111 mutants. Our preliminary results indicate that abnormal morphology of the brain and the source of stress on tissues may be partially due to over-proliferation of cells. Future experiments will examine laminin-111 mutants for epithelial integrity and localization of junctional proteins. We predict that our long-term findings will impact understanding of developmental disease and the future of tissue engineering and regenerative medicine.