CALMODULIN REGULATION OF LIGHT ADAPTATION AND STORE-OPERATED DARK CURRENT IN DROSOPHILA PHOTORECEPTORS

Phototransduction in Drosophila occurs through inositol lipid signalin g that results in Ca2+ mobilization. In this system, we investigate th e hitherto unknown physiological roles of calmodulin (CaM) in light ad aptation and in regulation of the inward current that is brought about by depletion of cellular Ca2+ stores, To see the effects of a decreas ed Ca-CaM content in photoreceptor cells, we used several methods, Tra nsgenic Drosophila P[ninaC(Delta B)] flies, which have CaM-deficient p hotoreceptors, were studied, The peptide inhibitor M5, which binds to Ca-CaM and prevents its action, Tvas applied, A Ca2+-free medium, whic h prevents Ca2+ influx and thereby diminishes the generation of Ca-CaM , was used, The decrease in the Ca-CaM level caused the following effe cts, (i) Fluorescence of Ca2+ indicator revealed an enhanced light-ind uced Ca2+ release from internal stores, (ii) Measurements of the light -induced current in P[ninaC(Delta B)] cells showed a reduced light ada ptation. (iii) Internal dialysis of M5 initially enhanced excitation a nd subsequently disrupted the light-induced current. (iv) An inward da rk current appeared after depletion of the Ca2+ stores with ryanodine and caffeine, Importantly, application of Ca-CaM into the photorecepto r cells prevented all of the above effects, We propose that negative f eedback of Ca-CaM on Ca2+ release from ryanodine-sensitive stores medi ates light adaptation, is essential for light excitation, and keeps th e store-operated inward current under a tight control.