• DOI:10.1006/mcne.2000.0846
• Corpus ID: 23861204

Normal Phototransduction in Drosophila Photoreceptors Lacking an InsP3 Receptor Gene

@article{Raghu2000NormalPI,
  title={Normal Phototransduction in Drosophila Photoreceptors Lacking an InsP3 Receptor Gene},
  author={Padinjat Raghu and Nansi Jo Colley and Rebecca Webel and Tracy James and Gaiti Hasan and Michal Danin and Zvi Selinger and Roger C. Hardie},
  journal={Molecular and Cellular Neuroscience},
  year={2000},
  volume={15},
  pages={429-445}
}

• P. Raghu, N. Colley, +5 authors R. Hardie
• Published 1 May 2000
• Biology
• Molecular and Cellular Neuroscience

The Drosophila light-sensitive channels TRP and TRPL are prototypical members of an ion channel family responsible for a variety of receptor-mediated Ca(2+) influx phenomena, including store-operated calcium influx. While phospholipase Cbeta is essential, downstream events leading to TRP and TRPL activation 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 known InsP(3)R 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 Ca(2+), light adaptation, and Ca(2+) release from internal stores all being normal. Using the specific TRP channel blocker La(3+) we demonstrated that both TRP and TRPL channel functions were unaffected. These results indicate that InsP(3)R-mediated store depletion does not underlie TRP and TRPL activation in Drosophila photoreceptors.