The inner ear is an internalized structure that is formed by the induction of the surface ectoderm.  Once specified, these cells undergo coordinated cellular changes that enable tissue level morphogenesis to form the inner ear: The inner ear cells thicken to become pseudostratified and subsequently invaginate and bend to give rise the otic cup. Throughout this process the otic ectoderm is contiguous with the surface ectoderm, however the border region between surface and otic ectoderm buckles to form folds. As the otic pit further deepens the folds are pushed together, until these folds fuse with each other, separating the otic and surface ectoderm. The question is how a single epithelium can be remodeled during fusion and subsequent separation? My project aims to characterise these steps.

I have found that the otic ectoderm and the surface ectoderm send out actin-based protrusions which recognize their counterparts from the opposing side. This is unusual for an epithelial cell. These filopodia seems to aid a zippering process in bring the folds close together. Analysis of the expression of different adhesion molecules and junctional proteins at this fusion point before and after the closure process; shows that the cells mediating the fusion have an altered shape and localization of junctional components. This data suggests that cells in the folds lose some of their epithelial character, enabling junctional rearrangements which aid in the separation and segregation of the otic and surface ectoderm. I am currently investigating the molecular mechanism underlying partial conversion of epithelial character in the otic folds.