Every cell in the body extends tiny, finger-like probes called filopodia to sense its surroundings, steer movement, and connect with neighbours—but no one knows exactly how they form. This project aims to solve that basic puzzle by watching filopodia assemble in a test tube, using frog egg extracts and artificial membranes to recreate the process outside a living cell. Understanding filopodia formation matters because these structures are fundamental to how neurons wire the brain, how wounds heal, and how pathogens like viruses force their way into cells. The researcher will focus on retinal ganglion cells—neurons that connect the eye to the brain—to see how lipid signals and endocytosis control where and when filopodia sprout during axon guidance and injury recovery. This is fundamental science. There is no immediate medical application. But knowing the molecular mechanics of filopodia could eventually allow researchers to manipulate cell movement and adhesion therapeutically—for example, encouraging nerve regrowth after injury or blocking pathogen entry. Past discoveries in actin regulation have already led to drugs that stop cancer cells from spreading; this work fills in the basic blueprint that makes such interventions possible.
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Filopodia are finger-like actin rich projections from cells that are ubiquitously present during cell movement, are involved in cell connectivity, and are hijacked for internalization by pathogens. We established a cell-free system of filopodia-like structure formation using supported lipid bilayers and frog egg extracts, which has generated hypotheses about where and when filopodia form. My first aim is to discover how endocytosis and phosphoinositide lipid metabolism contribute to the time and place of filopodia formation and suppression in retinal ganglion cell neurons. We will examine the timing and contributions of neurotrophic factor signalling through PI(4,5)P2, PI(3,4,5)P3, PI(3,4)P2 and PI(3)P to membrane deformation and filopodial protrusion. We will explore filopodia in axon guidance, terminal arborization and synaptogenesis, and recovery from neuronal injury. My second aim is to identify the proteins needed for formation of filopodia-like structures to increase our understanding of the molecular mechanisms that determine filopodia function in cells. Where filopodia form determines the direction of cell movement, their length determines the extent of signal sensitivity and their lifetime determines the strength of signaling or duration of migration and adhesion. Our molecular and cellular studies may also give us information needed to manipulate actin regulation therapeutically.
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