Heterozygotes have a blistered wing and ectopic vein phenotype.

Homozygotes die at the beginning of the first larval instar stage because the larvae cannot exit from the chorion. The larvae are deformed with stunted growth. The sclerotised mouthparts and denticle belts develop normally.

Intermediate second site non-complementing phenotype with zip^Ebr and zip^mhc-c6.1 : malformed phenotype penetrance 25-75%.

Shows no maternal enhancement of dpp^hr4.

The tracheal phenotypes previously reported for this deficiency in FBrf0051997 and FBrf0072461, where the primary branches are disrupted and discontinuous, are due to the deletion of a gene other than bs, or more than one gene in the region.

Shows a haploinsufficient ectopic wing vein phenotype.

Midgut development of mutant embryos is wild type.

Heterozygotes with T(2;3)God¹ are inviable.

Progeny of the genotype zip/Df(zip) exhibit the mlf phenotype (malformed syndrome), wing malformations and leg defects, at a penetrance of 14--35%.

Wing venation phenotype like Df(2R)Px1. Thickening of L5 at posterior crossvein produces a vesicle, as in bs. More extreme in female. homozygous lethal