Abstract
SummaryThe most prominent developmental function attributed to the extracellular matrix (ECM) is cell migration. While cells in culture can produce ECM to migrate, the role of ECM in regulating developmental cell migration is classically viewed as an exogenous matrix presented to the moving cells. In contrast to this view, we show here that Drosophila embryonic hemocytes deposit their own laminins in streak-like structures to migrate efficiently throughout the embryo. With the help of transplantation experiments, live microscopy, and image quantification, we demonstrate that autocrine-produced laminin regulates hemocyte migration by controlling lamellipodia dynamics, stability, and persistence. Proper laminin deposition is regulated by the RabGTPase Rab8, which is highly expressed and required in hemocytes for lamellipodia dynamics and migration. Our results thus support a model in which, during embryogenesis, the Rab8-regulated autocrine deposition of laminin reinforces directional and effective migration by stabilizing cellular protrusions and strengthening otherwise transient adhesion states.
Highlights
Cell migration plays a key role in a wide variety of biological phenomena that take place both during embryogenesis and in the adult organism
By combining live imaging with transplantation experiments and quantification analysis, we show that laminins are required for all steps of hemocyte migration throughout the embryo
We further demonstrate that autocrine-produced laminin enhance hemocyte migration by regulating lamellipodia dynamics and stability
Summary
Cell migration plays a key role in a wide variety of biological phenomena that take place both during embryogenesis and in the adult organism. There are numerous cases where organ or tissue formation depends upon the migration of primordial cells over large distances. Cell migration is essential for immune cells to monitor the body and for epithelial cells to heal a wound This fascinating behavior, which involves a large variety of intricately coordinated and controlled processes in normal cells, becomes destructive and damaging when acquired by cancerous cells. Experiments in cell culture have suggested that both exogenous and endogenous laminins may contribute to cell migration This is the case for a variety of tumor cells, including melanomas and gliomas. The use of produced laminins during cell migration has not been demonstrated in embryos or adults
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