Fig. 7. Loss of RhoA function causes defects in DE-cadherin localization and epidermal cell polarity. Embryos expressing RhoA^N19 driven by enGAL4 (indicated by bars) that were stained either with an antibody against DE-cadherin (A-D) or anti-ß_Heavy-spectrin (E-G). (A) RhoA^N19 expression causes loss of cell surface DE-cadherin at dorsal closure stages. Higher magnification images show complete loss of DE-cadherin surface staining is first apparent in ventral epidermal cells (C), when compared with the dorsal epidermis (B). (D) At earlier stages, punctate spots of DE-cadherin staining fail to coalesce into bands of apical staining in cells expressing RhoA^N19. (E) Lateral view of a stage 12 embryo; RhoA^N19-expressing cells lose apicolateral staining of ß_Heavy-spectrin. (F) Dorsal view of a stage 11 embryo showing loss of ß_Heavy-spectrin in RhoA^N19-expressing stripes at the ventral midline (midline indicated by an arrow). (G) Later, loss of apicolateral staining is clearly seen in RhoA^N19-expressing leading edge cells (arrowheads) that push beyond wild type neighbors. (H) DE-cadherin staining of a stage-14 RhoA mutant embryo depicting leading edge disorganization, but no loss of DE-cadherin staining. (J) At stage 15, when dorsal closure is complete, some RhoA mutants exhibit loss of cell surface DE-cadherin at sites of dorsal puckering (arrows; compare with wild-type embryo, I).