Ttd14^P75L mutant eye clones are unable to internalize the ion channel trpl.

Defects in light-dependent trpl localisation are seen in Ttd14^P75L mutant flies. In Ttd14^P75L mutant eye clones of 1-day old flies kept in darkness, trpl is correctly located in the rhabdomere but, unlike in controls, the amount of trpl at the rhabdomere is reduced the longer the flies remain in the dark. Upon illumination with orange light, the amount of trpl that moves to the cell body is reduced compared with wild type, with no movement at all when the flies are retained in the dark until 7 days. When the flies are returned to the dark after 16 hours of exposure to light, the recycling of trpl from the cell body back to the rhabdomere is severely impaired in 3 and 7 day old flies.

No obvious differences in electroretinogram recordings are seen in Ttd14^P75L mutant eye clones in flies kept in the dark for 7 days.

In a 12 hours light/12 hours dark cycle Ttd14^P75L mutant eye clones exhibit a decline in electroretinogram (ERG) amplitude compared with controls, and an almost abolished photoresponse after 14 days. This phenotype is unaffected by a vitamin A-deprived diet in 21 day old flies. Ttd14^P75L mutant flies kept in constant darkness for 21 days also display a reduction in ERG amplitude, but to a lesser extent.1G

Severe degeneration of photoreceptor cells is seen in Ttd14^P75L mutant flies keep in a 12 hours light/12 hours dark cycle for 21 days. Most rhabdomeres of photoreceptor cells R1-6 and R7 are affected. Degeneration is first detected at 7 days and almost all rhabdomeres are absent by 21 days. Degeneration is less when the flies are kept in the dark for 21 days: the R7 cell is frequently affected but almost all rhabdomeres of R1-6 cell remain intact. Degeneration is unaffected by a vitamin A-deprived diet. No photoreceptor degeneration is seen when the flies are kept in the dark for 7 days followed by 16 hours of orange light stimulation.