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.
Published Version
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