Imprecise excision of P{PZ}18w00053 generates a large deletion downstream of a partial P-element, that removes most, if not all, of the 18w open reading frame.
18wΔ21 mutant follicle cells exhibit delays in migration. Posterior migration of main body follicle cells is normally complete by early stage 10A. However, 18wΔ21 mutant follicle cell clones are still migrating posteriorly at this stage (a process normally completed by the end of stage 9). Even a small 18wΔ21 mutant clonal area disrupts and delays normal migration, with mutant dorsal cells having neither undergone the normal flattening nor begun to migrate centripetally. Border cell migration appears normal, even if they are part of a mutant clone.
Eggs laid by 18wΔ21 mutant females are both shorter and rounder than in wild-type. These eggs do not differ in volume compared to controls (i.e. there is an increase in width to compensate for length). Dorsal appendage morphogenesis appears disrupted in these embryos, with reduced or absent paddles.
The rate of successful hatching among normally hydrated eggs laid by females carrying 18wΔ21 clones is reduced by 20-40% relative to parallel wild-type collections.
