Normal phototransduction in Drosophila photoreceptors lacking an InsP₃ receptor gene

Abstract

The Drosophila light-sensitive channels TRP and TRPL are prototypical members of an ion channel family responsible for a variety of receptor-mediated Ca²⁺ influx phenomena, including store-operated calcium influx. While phospholipase Cβ is essential, downstream events leading to TRP and TRPL activation remain unclear. We investigated the role of the InsP₃ receptor (InsP₃R) by generating mosaic eyes homozygous for a deficiency of the only known InsP₃R gene in Drosophila. Absence of gene product was confirmed by RT-PCR, Western analysis, and immunocytochemistry. Mutant photoreceptors underwent late onset retinal degeneration; however, whole-cell recordings from young flies demonstrated that phototransduction was unaffected, quantum bumps, macroscopic responses in the presence and absence of external Ca²⁺, light adaptation, and Ca²⁺ release from internal stores all being normal. Using the specific TRP channel blocker La³⁺ we demonstrated that both TRP and TRPL channel functions were unaffected. These results indicate that InsP₃R-mediated store depletion does not underlie TRP and TRPL activation in Drosophila photoreceptors.