Cell migration is an interesting behavior that serves various functions during tissue morphogenesis and also in certain disease conditions including cancer. We have gained insight into the mechanisms of cell motility by studying the migration of single cells in vitro yet in recent years, studies on several epithelial cancers have provided evidence that clusters of metastatic cells invade more efficiently than individual cells. Therefore, it is of critical importance to understand the mechanisms of collective motility in vivo. Over the years, the Montell lab has developed a genetically tractable model of Drosophila border cells to study collective migration of cell clusters in vivo. Using this model, we aim to understand how collectively migrating cells coordinate activities of various signaling pathways and proteins involved, to move forward in a group.

The Rho family of small GTPases, Rac, Rho and Cdc42 represent central nodes in the cytoskeletal and signaling networks that drive cell migration and function as an off/on switch through the process of phosphorylation. Here we have studied the role of nonmuscle myosin II (Myo-II, a downstream component of Rho signaling) during border cell migration. Using antibody staining in fixed tissues, we have seen the myosin regulatory light chain (spaghetti squash in Drosophila) expressed in a very distinct pattern during border cell migration. Live imaging unveils that this pattern is very dynamic in nature. Knocking down Myo-II using RNAi displays a range of phenotypes including detachment failure, incomplete migration, cluster splitting and protrusion defects. Currently, we are knocking down Myo-II selectively in a subset of cluster to analyze the cell type specific effects of Myo-II in border cell migration. Overall, our study highlights a vital role of Myo-II in collective border cell migration and could also potentially contribute to further our understanding of collective chemotaxis in metastasis.