03-P005 Zebrafish epiboly as a model of vertebrate embryonic cell rearrangement

model in which cytoskeletal dynamics can be analysed with the wide range of genetic strategies and tools available for Drosophila. Morphological features and cytoskeletal dynamics closely resemble those of vertebrate GCs, suggesting this model to be of high translatable value. We will report subcellular roles of the actin-microtubule linker molecule Short stop (Shot; homologue of ACF7 and BPAG1) which regulates neuronal MT organisation and axon length in dependence of various F-actin regulators. Vice versa, Shot influences also F-actin organisation, as illustrated by its impact on filopodia formation. In this context, we have addressed basic mechanisms of filopodia formation in Drosophila GCs and show that Arp2/3and formin-dependent mechanisms of filopodia formation clearly co-exist. If both nucleators are knocked out genetically, F-actin (and consequently filopodia) can be essentially eliminated from such neurons – to our knowledge the first time such a condition has been achieved in any cell. Genetic interaction studies couple filopodia-promoting functions of both nucleators to the activity of enabled, which is itself essential for filopodia formation. In contrast, activity of the G-actin binding molecule profilin is important mainly for filopodia length, although genetic interaction with enabled suggests also a facilitating role in filopodia formation. Supported by: BBSRC, Wellcome Trust, FCT.