garz^Δ137 homozygous and garz^Δ137/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.

garz^Δ137 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 garz^Δ137 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 garz^Δ137 mutant embryos.

Salivary gland luminal length is unaffected in garz^Δ137 mutant embryos.

Luminal deposition defects and protein retention in intracellular compartments, accompanied by a reduced luminal diameter are apparent in garz^Δ137 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 garz^Δ137 mutants. The morphology of septate junctions appears wild-type in garz^Δ137 mutants. Compared with wild-type, the apical membrane domains of tracheal cells in garz^Δ137 mutant embryos are irregular and smaller. garz^Δ137 mutant embryos exhibit severe morphological defects in cellular compartments, with malformed endoplasmic reticulae.

Before the death of homozygous garz^Δ137 mutant individuals, the tracheal lumen collapses. Besides a reduction in luminal diameter, chitin cables organise aberrantly inside the tracheal lumen in garz^Δ137 mutants.

Epidermal secretion of the cuticle is disturbed to various degrees in garz^Δ137 mutants.

garz[+]/garz^Δ137 is a non-enhancer of abnormal neuroanatomy | third instar larval stage phenotype of Arfip⁷¹/Arfip¹²