Cell delamination is a morphogenesis process essential for organ formation during animal development. For instance, individual neural crest cells in vertebrates delaminating from the original position give rise to many kinds of cell types, including melanocytes, muscle cells, neurons, and glia; and pancreatic endocrine cells delaminate to form the Langerhans islets in the pancreas. Due to the importance of this morphogenetic movement, we want to study the cellular and molecular mechanism underlying cell delamination. We established Drosophila embryonic neuroblast delamination as a genetically and optically tractable system.

Through live imaging of the Drosophila embryo neuroectoderm, we demonstrate that myosin network forms dynamic flows and pulses in both delaminating neuroblas...[ Read more ]

Cell delamination is a morphogenesis process essential for organ formation during animal development. For instance, individual neural crest cells in vertebrates delaminating from the original position give rise to many kinds of cell types, including melanocytes, muscle cells, neurons, and glia; and pancreatic endocrine cells delaminate to form the Langerhans islets in the pancreas. Due to the importance of this morphogenetic movement, we want to study the cellular and molecular mechanism underlying cell delamination. We established Drosophila embryonic neuroblast delamination as a genetically and optically tractable system.

Through live imaging of the Drosophila embryo neuroectoderm, we demonstrate that myosin network forms dynamic flows and pulses in both delaminating neuroblasts and their non-delaminating neighbors. Quantitative analysis shows that medial myosin contractions correlate with apical area changes. The medial myosin pulses exhibit higher amplitude and frequency in the delaminating neuroblasts compared with their neighbors. Drug inhibition and genetic experiments indicate that medial myosin pulses are required to drive neuroblast delamination. The neuroblast singling out event is determined by lateral inhibition function exerted by Notch signaling. We further find that neuroblast delamination process is dependent on the transcriptional activity mediated by Notch intracellular domain (NICD).

To determine how Notch signaling regulates a highly dynamic and quantitatively refined myosin network, we compared transcriptomes of embryos injected with water and Delta dsRNA at the onset of neuroblast delamination and identified a set of differentially expressed genes. We then performed genetic screening from the gene list and identified several novel components regulating neuroblast delamination. We need to further verify their functions by checking the mutant phenotype of these genes.