Dynamin is a multi-domain GTPase that forms polymers along lipid surfaces and acts in multiple vesicular trafficking events. In addition to its well-known membrane fission function in endocytosis (1), C. elegans dynamin (DYN-1) is also known to promote regulate synaptic vesicle transport and cytokinesis (2,3). Recent studies found that DYN-1 is essential for the removal of apoptotic cells (3,4,5). In C. elegans, apoptotic cells are swiftly engulfed by surrounded tissues and degraded inside phagosomes. The swift engulfment and degradation of apoptotic cells rely on the efficient transport and fusion of intracellular vesicles to phagocytic cups and maturing phagosomes. DYN-1 is localized to the surfaces of extending pseudopods and nascent phagosomes in response to the signaling from phagocytic receptor CED-1, and promotes vesicle delivery to these regions. To understand the distinct roles of DYN-1''s self-assembly and GTP hydrolysis for the removal of apoptotic cells, we analyzed two classes of missense mutations of DYN-1. In vitro, Class I mutant DYN-1 fails to bind and/or hydrolyze GTP. In contrast, a Class II mutation specifically affects DYN-1''s self-assembly along lipid surfaces. Our genetic and cell biological studies in C. elegans generated multiple lines of evidence to indicate that DYN-1 undergoes self-assembly in vivo. Furthermore, we have found that self-assembly is essential for DYN-1''s association to the surfaces of pseudopods and phagosomes and the apical surface of intestinal cells, whereas the dissociation of DYN-1 from its target membranes is GTP-dependent. We propose that the self-assembly and GTP hydrolysis activities of DYN-1 play important and distinct roles in regulating DYN-1''s dynamic association to target membranes, an event known to be essential for DYN-1''s activity in apoptotic-cell removal and likely to be so for other cellular functions of DYN-1. References: 1.Grant, B. and D. Hirsh, Mol Biol Cell, 1999.10: 4311-26. 2.Clark, S.G., et al., Proc Natl Acad Sci USA, 1997. 94: 10438-43. 3.Thompson, H.M., et al., Current Biology, 2008.12: 2111-2117. 4.Yu, X., et al., Dev Cell, 2006. 10: 743-57. 5.Yu, X., et al., PLoS Biol, 2008. 6: e61. 6.Kinchen, J.M., et al., Nat Cell Biol, 2008. 10: 556-66.