The epithelial to mesenchymal transition (EMT) is an important process 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 distributed across the apical surface of the delaminating neuroblasts a...[ Read more ]

The epithelial to mesenchymal transition (EMT) is an important process 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 distributed 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 neighbors, the medial pulses exhibit higher amplitudes and frequency in the delaminating cells than their neighbors. Interestingly, when the embryos are injected with low-dose CytoD to deplete the medial myosin pulses, single presumptive neuroblasts still undergo pulsatile apical constriction but would 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. Notch signaling pathway is important for the neuroblast cell fate specification. When Notch signaling pathway was disrupted, we observed many cells instead of one cell delaminate together in one cluster with higher and increasing myosin intensity compared with the non-delaminating neighboring cells, indicating that Notch pathway may participate in regulating the myosin-driven apical constriction process in delaminating neuroblasts.