Abnormal olfactory behaviour, but recovery kinetic is not significantly delayed and defective response in olfactory jump assay that is reduced further in the dark. Light induced degeneration of photoreceptor cells. No EAG defect.
Homozygotes show abnormal trap-entry with food medium or ethyl acetate as the stimulus, and a defective response (to ethyl acetate, propionic acid or benzaldehyde) in a chemosensory jump assay. Retinal depolarisation is defective in homozygotes; the "on" and "off" transients are missing. Giant fibre pathway physiology appears normals.
Poor odor responses in tests involving an olfactory trap; entry into such traps was subnormal when odorant was food medium or ethyl acetate. Phenotype also subnormal in odor-induced jump responses (using ethyl acetate, propionic acid, or benzaldehyde as stimulant). Electroretinogram abnormal; very weak light induced depolarization and no light-on or light-off transients.
rdgBota1 has eye photoreceptor cell phenotype, suppressible by trp1
rdgBota1 has ommatidium phenotype, suppressible by trp1
rdgBota1 has eye photoreceptor cell phenotype, non-suppressible by inaC2
rdgBota1 has ommatidium phenotype, non-suppressible by inaC2
inaC2 does not significantly alter the deep pseudopupil loss of rdgBota1 flies and fails to suppress the photoreceptor degeneration and ommatidial disorganisation seen in these flies at 6 days after eclosion. trp1 slows the initiation of deep pseudopupil loss of rdgBota1 flies and dramatically suppresses photoreceptor degeneration and ommatidial disorganisation in these flies.
The olfactory and ERG phenotypes of rdgBota1 cosegregate.