Isolation of adaptation mechanisms and photopigment spectra by vitamin A deprivation inDrosophila

Summary

Intense short wavelength adaptation converts rhodopsin to a long wavelength absorbing stable metarhodopsin and inactivates R1–6 photoreceptors inDrosophila. In addition to decreasing sensitivity, vitamin A deprivation eliminates this short wavelength induced R1–6 inactivation. A model (Fig. 4) explains this adaptational difference of vitamin A deprivedDrosophila (from normally-reared or high vitamin A supplemented flies) in terms of decreasing photopigment quantity without decreasing membrane adaptation mediating channels. The data and model suggest that 1) photopigment and membrane processes are separate; 2) transduction and adaptational mechanisms are different; and 3) maximal adaptation establishes a steadystate wavelength-specific rhodopsin to metarhodopsin ratio. Sensitivity as a function of wavelength for maximal adapting stimuli was obtained from vitamin A deprivedDrosophila (Fig. 3). These data reflect relative rhodopsin levels. They were used to derive a measure related to spectral sensitivity ofin vivo metarhodopsin spectral absorption characteristics (Fig. 5). The presently reported metarhodopsin spectral function has certain advantages over previously reported electrophysiologically-based functions. It differs fromin vitro data by having an ultraviolet maximum and a shorter wavelength visible maximum. This finding is consistent with current theory on fly vision. The data obtained from vitamin A deprivedDrosophila are similar to data fromCalliphora andMusca; possible adaptational differences among different fly species may be explained by the model which explains differences betweenDrosophila in the vitamin A deprived vs. enriched conditions.