garzΔ137 homozygous and garzΔ137/Df(2R)Exel6061 transheterozygous animals develop until the end of embryogenesis but fail to hatch and subsequently die. Moreover, mutant individuals exhibit asynchronous development and considerable retardation in comparison with wild-type controls.
garzΔ137 embryos exhibit a reduction in cis-Golgi network compartments in salivary gland cells. Vesicles secreting electron-dense ECM material, which are normally numerous close to the apical membrane of salivary gland cells at stage 16, are entirely absent in garzΔ137 mutant embryos. At the same time, the highly enriched rough endoplasmic reticulum (ER) is absent, with the ER appearing as a 'bloated balloon'. The formation of zonulae adherentes and septate junctions is not affected in garzΔ137 mutant embryos.
Salivary gland luminal length is unaffected in garzΔ137 mutant embryos.
Luminal deposition defects and protein retention in intracellular compartments, accompanied by a reduced luminal diameter are apparent in garzΔ137 mutant embryonic trachea. The clearance of liquid and replacement with gas are visible in wild-type animals as late as stage 16, but is inhibited in garzΔ137 mutants. The morphology of septate junctions appears wild-type in garzΔ137 mutants. Compared with wild-type, the apical membrane domains of tracheal cells in garzΔ137 mutant embryos are irregular and smaller. garzΔ137 mutant embryos exhibit severe morphological defects in cellular compartments, with malformed endoplasmic reticulae.
Before the death of homozygous garzΔ137 mutant individuals, the tracheal lumen collapses. Besides a reduction in luminal diameter, chitin cables organise aberrantly inside the tracheal lumen in garzΔ137 mutants.
Epidermal secretion of the cuticle is disturbed to various degrees in garzΔ137 mutants.