Journal
JOURNAL OF NEUROSCIENCE
Volume 26, Issue 49, Pages 12816-12825Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3673-06.2006
Keywords
TRP channels; phototransduction; Drosophila; calcium; retinal degeneration; PIP2
Categories
Funding
- NEI NIH HHS [EY10852, R01 EY010852, EY08117, R01 EY008117] Funding Source: Medline
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Drosophila phototransduction serves as a model for phosphoinositide ( PI) signaling and for characterizing the mechanisms regulating transient receptor potential (TRP) channels in vivo. Activation of TRP and TRP-like (TRPL) requires hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2), resulting in the generation of inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). Although a role for IP3 has been excluded, TRP channels have been proposed to be activated by either a reduction of inhibitory PIP2 or production of DAG/polyunsaturated fatty acids. Here, we characterize a protein, phosphatidylinositol synthase (dPIS), required for a key step during PIP2 regeneration, the production of phosphatidylinositol. Overexpression of dPIS suppressed the retinal degeneration resulting from two other mutations affecting PIP2 cycling, rdgB (retinal degeneration B) and cds (CDP-diacylglycerol synthase). To characterize the role of dPIS, we generated a mutation in dpis, which represented the first mutation in a gene encoding a PI synthase in an animal. In contrast to other mutations that reduce PIP2 regeneration, the dpis(1) mutation eliminated all PI synthase activity in flies and resulted in lethality. In mosaic animals, we found that dPIS was essential for maintaining the photo response. Because the dpis(1) mutation eliminates production of an enzyme essential for PIP2 regeneration, our data argue against activation of TRP and TRPL through a reduction of inhibitory PIP2.
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