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The optic fissure, is a consequence of the morphogenetic formation of the vertebrate retina. During eye morphogenesis, forebrain tissue slated to become the eye evaginates to form the optic vesicle. A subsequent invagination of the optic vesicle shapes this epithelial sheet into a bi-layered optic cup. A consequence of this folding is the fissure that remains open at the ventral part of the optic cup, called the optic (choroid) fissure.
The fissure remains open during early retinal development to allow for establishment of vasculature inside the retina. Once vasculature has invaded, the fissure closes to ensure a continuous retinal tissue structure. Failure of the fissure to close has significant implications on retinal function and presents in human patients as the congenital condition coloboma. Patients with coloboma range from partial to complete loss of vision in the affected eye, depending how far the fissure remains open in regards to the optic stalk.
In our lab, we are using zebrafish to both observe optic fissure closure as well as model human coloboma patient mutations. Using long-term live confocal microscopy, we can observe, characterize and quantitate cellular behaviours as well as morphogenetic movements of cells, epithelial sheets and entire tissues. By applying novel cutting edge genome editing techniques we can generate transgenic fish to label specific cell populations or to introduce mutations in coloboma candidate genes. Ultimately we strive to understand the molecular mechanisms driving and regulating this important and dynamic developmental event. The project will be focusing on analyzing molecular mechanisms related to cell-cell interaction and fusion, including actin and microtubule regulation, cell polarity and extra cellular matrix (ECM) remodelling. There will be a heavy emphasis on high quality microscopy and molecular biology.