Fps85D^gof embryos exhibit a number of defects. The embryos fail to complete dorsal closure; dorsal closure starts to arrest at stage 13, with only the most anterior and posterior segments meeting at the dorsal midline at stage 16. The leading edge and dorsal epidermal cells fail to elongate while the actomyosin cable still forms and creates a straightened leading edge, although this is reduced in thickness compared to wild type. The F-actin-rich filopodia that extend from the leading edge are also much less extensive in Fps85D^gof embryos than in wild type. Fps85D^gof embryos show aberrant midline crossing of axons in the CNS and the amnioserosa is also affected. Amnioserosal cells exhibit more lamellipodia, F-actin staining is much less concentrated at the cell-cell junctions, and the cell cortices are irregular. However, contraction of isolated amnioserosal cells still occurs.

Expression of Fps85D^RB.Scer\UAS under the control of Scer\GAL4^da.G32, Scer\GAL4^wex1.for and Scer\GAL4^wex1.rev in a Fps85D^gof background enhances the axon midline-crossing defect of Fps85D^gof embryos.