pck^VE896 homozygous stage 16 and 17 embryos show a defective tracheal transepithelial barrier as, unlike in controls, a dye injected into the haemocoel diffuses into the tracheal lumen.

Germline clone analysis revealed that embryos lacking maternal pck function form a normal tracheal system and develop into fertile adults. Zygotic mutant phenotype is indistinguishable from that of embryos lacking both maternal and zygotic component pck. Transepithelial barrier function is affected - rhodamine labelled dextran diffuses across the epithelial sheet. Cells of the dorsal tracheal trunk have an irregular and stretched shape. Subcellular localization of actin and tubulin, and the polarization of the microtubule cytoskeleton, appear normal.

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.

embryonic lethal no maternal effect in homozygous germ-line clones