Calcium influx via TRP channels is required to maintain PIP2 levels in Drosophila photoreceptors

R C Hardie, P Raghu, S Moore, M Juusola, R A Baines, S T Sweeney, Sean Sweeney

Research output: Contribution to journalArticlepeer-review


The trp (transient receptor potential) gene encodes a Ca2+ channel responsible for the major component of the phospholipase C (PLC) mediated light response in Drosophila. In trp mutants, maintained light leads to response decay and temporary total loss of sensitivity (inactivation). Using genetically targeted PIP2-sensitive inward rectifier channels (Kir2.1) as biosensors, we provide evidence that trp decay reflects depletion of PIP2. Two independent mutations in the PIP2 recycling pathway (rdgB and cds) prevented recovery from inactivation. Abolishing Ca2+ influx in wild-type photoreceptors mimicked inactivation, while raising Ca2+ by blocking Na+/Ca2+ exchange prevented inactivation in trp. The results suggest that Ca2+ influx prevents PIP2 depletion by inhibiting PLC activity and facilitating PIP2 recycling. Without this feedback one photon appears sufficient to deplete the phosphoinositide pool of approximately 4 microvilli.
Original languageEnglish
Pages (from-to)149-59
Number of pages11
Issue number1
Publication statusPublished - 2001


  • Animals
  • Biosensing Techniques
  • Calcium
  • Calcium Channels
  • Calcium Signaling
  • Culture Media
  • Drosophila Proteins
  • Drosophila melanogaster
  • Insect Proteins
  • Membrane Potentials
  • Mutation
  • Phenotype
  • Phosphatidylinositol 4,5-Diphosphate
  • Photoreceptor Cells, Invertebrate
  • Potassium Channels
  • Potassium Channels, Inwardly Rectifying
  • Transient Receptor Potential Channels
  • Vision, Ocular

Cite this