Cell migration is an essential biological process. In addition to being required for development and maintenance, cell motility also contributes to human disease. For example cancer metastasis is dependent on tumor cells gaining motility and traveling
to secondary sites within the body. Cell motility requires the formation of protrusive structures including filopodia and lamellipodia. The formation of these structures requires rearrangement and coordinated organization of the actin cytoskeleton.
Here I show that Drosophila Clic, a member of the CLIC family, contributes to the formation of filopodia by regulating the nucleation and elongation of these structures.
This is done by examining the localization of Clic and genetic interactions with known cytoskeleton regulators. I show that there are three phases of filopodia formation,supported by the observed genetic interactions. I provide evidence that Clic is
involved in all three phases of filopodia formation and interacts with Cell division cycle 42 (Cdc42), Diaphanous (Dia), Wiskott - Aldrich syndrome protein (WASp), the Actin related protein (Arp) 2/3 complex, Moesin (Moe), and Enabled (Ena). I also show that Clic may contribute to in vivo cell migration through the study of hemocyte
migration in Drosophila embryos.