The epithelial to mesenchymal transition (EMT) is a process important for organ formation, tissue homeostasis and tumor metastasis. We use Drosophila embryonic ventral nerve cord neural stem cells, the neuroblasts, as a model to study EMT events. In the neuroectoderm, for each proneural cluster of cells, one cell undergoes EMT, delaminates from the epithelium and becomes the neuroblast, while the surrounding cells remain as epithelial cells. Apical constriction is one of the key events during EMT, and in our project we aim at dissecting how the actin-myosin network drives apical constriction in a single cell delamination event.
Through imaging live embryos, we noticed that dynamic myosin loci and fibers are present across the apical surface of the delaminating neuroblasts as well as the neighboring non-delaminating cells. Quantitative analysis showed that medial myosin contractions correlate with apical cell area changes. Although the medial myosin contractile pulses are present in both delaminating neuroblasts and their non-delaminating neighbors, the medial pulses exhibit higher amplitudes and appear at higher frequency in the delaminating cells than their non-delaminating neighbors. Interestingly, when the embryos are injected with low-dose CytoD to deplete the medial myosin pulses, we noticed that the single presumptive neuroblasts still undergo pulsatile apical constriction but fail to maintain the cell area, reflex back and fail to effectively decrease their apical area over time. In these cells, the junctional myosin intensity increase precedes apical area decrease in one round of apical constriction, indicating that the junctional myosin plays a role in initiating apical constriction and the medial myosin might function to stabilize the cell shape in the delaminating neuroblasts.