DZIP1¹ homozygotes show impaired geotaxis response in bang assays, as all flies fail to reach the top of the tube after 30s. DZIP1¹/Df(3R)Exel8178 transheterozygotes show a more severe defect, with flies not only being unable to climb, but being completely immobile with held-up wings.

Cilia are almost completely absent in the chordotonal neurons of DZIP1¹ homozygous scolopidia. Whereas doublet microtubules are present and symmetrically organized at the basal body level, they fail to elongate along the transition zone, which is incompletely assembled and disorganized. No more axoneme-to-membrane linkers can be observed. Basal bodies are normally present at the dendrite distal tip, but there is a rapid disorganization of the axoneme, with its complete abrogation a few microns above the basal body.

DZIP1¹ homozygous and DZIP1¹/Df(3R)Exel8178 transheterozygous testes show a marked dispersion of the nuclei along the cysts and altered migration of sperm individualization complexes. Round spermatids of DZIP1¹ homozygotes occasionally exhibit axonemal defects, including missing microtubule central pairs, broken symmetry with each part of the axoneme being relocated along the mitochondria, or missing axonemes. More severe defects are observed in DZIP1¹/Df(3R)Exel8178 spermatid cysts (missing or broken axonemes), which are more prevalent in early spermatids than in late spermatids. In late DZIP1¹/Df(3R)Exel8178 cysts, there were significantly fewer spermatids per cyst than controls, but almost all remaining elongated spermatids show normal axonemes. Some DZIP1¹/Df(3R)Exel8178 spermatids exhibit aberrant growth of axonemal microtubules. Centriole docking in DZIP1¹ spermatocytes is impaired with partial docking of the centriole or docking to the plasma membrane of only one centriole of the pair; centrioles also present an altered/irregular cap in young spermatocytes, before centriole docking.