Figure 3. Dominant negative expression of Cdc42 causes severe DV defects.

(A-C) Stage 17 Hand-GAL4,UAS-GFP-moe (control) embryos in whole mount stained with anti-αSpectrin (A) and anti-GFP (B) in the heart region of the DV to show normal CB morphology and alignment at the dorsal midline. (C) is a merged image of (A) and (B). Overexpression of dominant negative Cdc42 (Cdc42 ^N17) (D-F) in the DV produces large holes (asterisks) within the heart. Anti-αSpectrin staining of the aorta (G-H) reveals abnormal CB morphology (arrowhead) in Cdc42^N17 mutants (H) compared to wild type (w¹¹¹⁸) aortas (G), albeit no CB contact defects as seen in the heart region (E). (I) Cdc42^N17 mutants maintain proper dorsal ectodermal closure, evident by anti-αSpectrin staining. (I) is the same embryo as shown in (D-F) at a different focal plane. (J-K) Overexpression of wild type Cdc42 (Cdc42^WT) does not cause any defects in the aorta (J) and results in only minor gaps (arrow) between Svp+ cells in the heart (K). (L) Overexpression of Cdc42^N17specifically in Svp+ CBs with Svp-GAL4 results in normal DV closure and CB morphology as apparent by anti-αSpectrin staining. See Table 1 for quantitative data.