The formin dDAAM is expressed in cardioblasts during heart morphogenesis and genetically interacts with Cdc42. (A) Antibody staining against dDAAM shows that it localizes to the membrane of all CBs including the Tinman-negative ostia cells. Tin⁺ pericardial cells do not express dDAAM (broken lines). Heart cells are visualized with tin^HE-Gal4 driving GFP. (B) Cdc42 and dDAAM genetically interact. The loss-of-function allele dDAAM1^Ex68 does not give rise to embryonic phenotypes (B) due to the maternal contribution of dDAAM. A large proportion (8/18) of Cdc42³, dDAAM^Ex68 double mutants show severe cardiac defects (B′) that are not observed in either single mutant, indicating that both genes interact during heart morphogenesis. (C) Strong expression of the C-terminal domains of dDAAM (CdDAAM), with tinD-,tinCΔ4-Gal4 Tin inducing ectopic heart lumina (arrowheads) that are positive for Dg (C′) and Slit (C″). (D) tinCΔ4-driven UAS-CdDAAM does not induce ectopic heart lumina (arrowheads) as shown by wild-type Mp localization.