Normal phototransduction in Drosophila photoreceptors lacking an InsP(3) receptor gene

The Drosophila light-sensitive channels TRP and TRPL are prototypical membe rs of an ion channel family responsible for a variety of receptor-mediated Ca2+ influx phenomena, including store-operated calcium influx. While phosp holipase CP is essential, downstream events leading to TRP and TRPL activat ion remain unclear. We investigated the role of the InsP(3) receptor (InsP( 3)R) by generating mosaic eyes homozygous for a deficiency of the only know n InsP(3)R gene in Drosophila. Absence of gene product was confirmed by RT- PCR, Western analysis, and immunocytochemistry. Mutant photoreceptors under went late onset retinal degeneration; however, whole-cell recordings from y oung flies demonstrated that phototransduction was unaffected, quantum bump s, macroscopic responses in the presence and absence of external Ca2+, ligh t adaptation, and Ca2+ release from internal stores all being normal. Using the specific TRP channel blocker La3+ we demonstrated that both TRP and TR PL channel functions were unaffected. These results indicate that InsP(3)R- mediated store depletion does not underlie TRP and TRPL activation in Droso phila photoreceptors.