Homozygous Cby1 and hemizygous Cby1/Df(3R)BSC805 mutants are viable, but mutant males appear to be hypo-fertile.
When compared with wild-type, homozygous Cby1 and hemizygous Cby1/Df(3R)BSC805 mutants display negative geotaxis defects.
Homozygous Cby1 and hemizygous Cby1/Df(3R)BSC805 mutants display defects in mechanosensation. Compared with wild-type, the antennal sound-evoked potentials (reflecting mechanotransduction in the antennal chordotonal organs) are strongly reduced in the mutants. Further, whereas most of the control antennae show a pulsatile response, many of the Cby1 antennae lack any response.
Embryos in the offspring of homozygous Cby1 mutant parents do not show any cuticular defects. Bristle number and distribution in Cby1 adults appear normal compared to wild-type.
Comparison of wild-type and Cby1 mutant chordotonal organs on adult legs or antennae reveals that cilia are missing in about a third of the mutant scolopidia. When ciliary profiles are present, characteristic ultrastructural defects are observed that are never seen in controls. The most frequent defect is a reduced number of microtubule doublets. In rare cases, extra doublets are observed, or the symmetry of the axoneme is abnormal. The majority of the homozygous Cby1 chordotonal cilia are ultrastructurally normal.
In homozygous Cby1 mutant flies, some of the basal body structures of chordotonal neurons are completely missing. Either completely interrupted symmetry or more subtle discontinuities in the microtubule associated structures are observed at the level of the ciliary transition zone. Discontinuities in the transition zone can also be observed on longitudinal sections in addition to membrane bulges that are never observed in controls. Basal bodies, though present in all neurons, are not positioned properly at the base of the cilia in some Cby1 mutant neurons. The ultrastructural defects observed in Cby1 flies are incompletely penetrant.
Differential interference contrast microscopy of live squashes of testes from Cby1 mutant males show no cellular defects in spermatocyte-stage cysts: all are composed of 16 cells. The number of spermatids in each mature cyst is reduced from testes of Cby1 mutants as revealed by electron-microscopy. An altered number of spermatids is sometimes seen in early spermatid cysts, suggesting a possible meiotic defect, however, meiosis defects do not seem to be prevalent in Cby1 testes.
No significant variations are seen in the ratio of nuclei-to-mitochondrial (Nebenkern) derivatives in Cby1 mutant onion-stage cysts, even though some aberrant spermatids can sometimes be observed.
In early Cby1 spermatid sections, mitochondrial derivatives with no axoneme can be observed, as well as axonemes with no visible mitochondria derivatives, which are never observed in controls. The axonemal ultrastructure in Cby1 mutants is characterised by partially penetrant but reproducible defects. Incomplete axonemal structures are found with a reduced number of microtubule doublets in the mutants.