Unlike wild-type, post stage 15 trachea in pck^EA97 homozygotes are unable to exclude from their lumens, a fluorescently labelled 10kDa dextran injected into the body cavity. This is consistent with these trachea lacking a functioning septate junction barrier. The primary tracheal branches of these embryos are extremely elongated, but have almost no diameter defects.

Early tracheal development, including primary branch budding and outgrowth and lumen formation and morphology occur normally during stages 11-14. Stage 16 embryos show a number of tracheal defects. These include an increased length of the dorsal trunk compared to wild type (with no accompanying increase in cell number), mild or no defects in the diameter of the dorsal trunk and moderate defects in the diameter of other primary branches. Irregular and variable tracheal tube morphologies, with local constrictions and/or dilations are seen in all major branches. The defects are first seen at stage 15.

Cuticle is poorly pigmented, denticle belts are incompletely developed although segmentation is normal. Tracheal trunks display sclerotized internal lesions. Hemizygotes display the classical bcd phenotype of a double abdomen.

embryonic lethal no maternal effect in homozygous germ-line clones