Time-lapse images of an adherens junction marker (AJM-1) tagged with GFP in a control C. elegans embryo during ventral enclosure early elongation (top panel) and in an nmy-2 (non-muscle myosin heavy chain) mutant embryo (bottom panel).
Morphogenesis is a term typically used to describe the development of tissues, which is essential for any multicellular organism. Mechanisms like the spreading, invagination, extension, or fusion of epithelia cells are achieved by dramatic changes in the actin-myosin cytoskeleton.
Formation of the epidermis in Caenorhabditis elegans occurs during mid-/late-embryogenesis, spans ~4 hours, and involves cell shape changes, migration and adhesion. Epidermal morphogenesis helps the embryo transform from an ovoid ball of cells into the elongated shape of a worm.
In the lab, we study ventral enclosure, when the ventral epidermal cells migrate to and adhere with their contralateral partners at the ventral midline to cover the embryo’s ventral surface in a single layer of epithelial cells. During this process, migration of the epidermal cells relies on the underlying neuroblasts (future neurons), underlining the importance of tissue-tissue communication for this process. While neuroblasts provide chemical cues to regulate epidermal cell migration, it is not known if they also provide mechanical forces (e.g. via non-muscle myosin-dependent contractility) that can influence this process. Intercellular networks of contractility in epidermal cells have been shown to regulate epidermal morphogenesis in other organisms, but it is not known if/how contractility in other tissues could influence epidermal morphogenesis. We are currently investigating the requirements for non-muscle myosin and its regulators in the neuroblasts, and how they can influence C. elegans epidermal morphogenesis.