Cell intercalation and migration mediated by actin contractility are key cellular behaviors in fusion of the mammalian secondary palate (344.2)

Abstract

Fusion of two distinct embryonic prominences is a process common to numerous developmental contexts and often requires the removal of an intervening epithelium. Upon fusion of the mammalian secondary palatal shelves, the resulting medial epithelial seam (MES) must be removed to allow formation of a continuous secondary palate. This problem has been studied at great length, leading to three main cellular explanations. Whereas considerable investigation has been made into epithelial to mesenchymal transition (EMT) and programmed cell death of the intervening epithelium as the definitive cellular mechanisms, the contribution of cell migration of the intervening epithelium in this process is not clear. By combining confocal live imaging in explant culture with functional molecular genetics in mice, we now provide direct evidence that cell migration is a key component of removal of the MES. Further, we find that integration of a disorganized multi‐layered epithelium into a shared single layer epithelium is an essential early step in secondary palate fusion. Both integration and migration of the MES requires an actin contractility pathway involving Rho Kinase (ROCK), Myosin light chain kinase (MLCK) and culminating with activation of Non‐muscle myosin IIA (NMIIA). Together, these data provide direct support for cell migration in removal of the MES, and allow us to begin to assemble a molecular pathway controlling this action.Grant Funding Source: Supported by R03 DE022818 from NIH/NIDCR