Stages 10B and early 11 of dorsal appendage morphogenesis proceed normally in bwk151/bwkΔ11 egg chambers. Defects in both roof and floor formation become evident in the developing dorsal appendage shortly after morphogenesis begins. Although apical constriction occurs normally in roof cells, the roof cell apices fail to reorganise from an almond shape into a normal triangular array by late stage 11. Instead, the roof cells form a blunt array, that even in stage 12, is abnormally short and/or wide. Floor cells begin to elongate normally, extending beneath the nascent roof in late stage 11, but they show defects in several subsequent stages; they frequently separate along their basolateral margins during tube formation, extend far too laterally and have apical gaps that result in an incomplete tube floor. Even when the roof population attains a normal length, the floor cells of the dorsal appendage primordium often extend too far laterally and have basal discontinuities. During anterior extension, the floor cell population becomes increasingly disorganised, often forking into large clefts. The roof cell population can also bifurcate. This bifurcation correlates with the secretion of prongs and spurs of chorion that project off the main dorsal appendage in the mutant. Defects are also seen in paddle formation; the mutant cells remain 27% more elongated during paddle formation than wild-type cells.
bwkΔ11, cic1 has lethal - all die during embryonic stage phenotype
bwkΔ11, cicD49 has partially lethal phenotype
bwkΔ11 combined with cic1 produces animals with a terminal phenotype. bwkΔ11, cicD49 animals are 'almost lethal' and have abnormal wings. These wings can have an extra wing vein tissue phenotype, where intervein cells acquire morphological features of vein cells at least partially. This extra tissue is usually close to the normal veins. This wings also have wing blisters. These animals also have defects in the male genitalia. The cuticle plates forming the genitalia are oriented in the opposite direction to those of wild-type. The addition of bwkΔ11 and vn1 fails to enhance the extra wing vein phenotype seen in cicD49/bwkΔ11 animals.
