rdhB1 animals exhibit defects in the function of abdominal lateral pentascolopidial chordotonal organ lch5 (in third instar larvae) and Johnston organ (in adults) mechanoreceptors compared to controls.
rdhB1 mutants are unable to produce rhodopsin after feeding on food containing either all-trans-retinal or all-trans-retinol.
rdhB1 mutants are able to synthesize normal levels of rhodopsin after being places on a diet supplemented with Β-carotene. However, in contrast to wild-type, levels of ninaE are reduced significantly in rdhB1 mutants after feeding on either all-trans-retinal or all-trans-retinol.
rdhB1 mutants exhibit an electrophysiological phenotype due to low levels of rhodopsin resulting in a prolonged depolarization afterpotential (PDA). A PDA can only be produced when functional rhodopsin is in a molar excess over arrestin, as in 2 day old wild-type and rdhB1 flies, and in 25 day old wild-type flies. Consistent with the 90% decrease in ninaE in 25 day old rdhB1 mutants, bright blue light does not produce a PDA in the mutant.
rdhB1 mutants, aged under a light/dark cycle for 30 days, exhibit rhabdomeres that are either smaller than in wild-type or absent. All seven rhabodmeres are present if the mutant flies are incubated in the dark for 30 days.
rdhB1 is rescued by Scer\GAL4rdhB/rdhBUAS.Tag:MYC
Expression of rdhBScer\UAS.T:Hsap\MYC under the control of Scer\GAL4rdhB rescues the level of rhodopsin in the developing eye in rdhB1 mutants to wild-type levels, so allowing bright blue light to produce a prolonged depolarization afterpotential, as in wild-type.
