S21-02. Regulation of TGF-beta signalling by Dapper2 in vertebrate development

We know a great deal about the mechanisms controlling common cellular processes, but still do not understand how cells communicate to ensure that they stretch in a coordinate manner. For instance, C. elegans embryonic morphogenesis relies on cell shape changes within the epidermis and on epidermis-muscles interactions. I will illustrate the importance of forces and tension during morphogenesis through two aspects. First, I will show that myosin II has an essential role only in a subset of epidermal cells, the lateral seam cells. Other epidermal cell types are maintained in a tension-relaxed mode by a myosin II negative regulator, and passively change shape by responding to tension exerted in seam cells. A model of elongation based on the physical properties of the cytoskeleton predicts that seam cells could indeed drive elongation alone. Second, combining genetic and biochemical approaches, we dissected how muscles help elongation (a 20-year old mystery in the field). We found that muscles exert mechanical tension on the epidermis, which is converted into a chemical signal by a protein kinase that when active phosphorylates the cytoskeleton (kinase activation involves two RhoGEFs and a small GTPase). Hence, mechanotransduction provides a mean to coordinate muscle and epidermis extension.