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Store-operated Ca 2+ entry (SOCE) occurs when loss of Ca 2+ from the endoplasmic reticulum (ER) stimulates the Ca 2+ sensor, STIM, to cluster and activate the plasma membrane Ca 2+ channel Orai (encoded by Olf186-F in flies). Inositol 1,4,5-trisphosphate receptors (IP 3 Rs, which are encoded by a single gene in flies) are assumed to regulate SOCE solely by mediating ER Ca 2+ release. We show that in Drosophila neurons, mutant IP 3 R attenuates SOCE evoked by depleting Ca 2+ stores with thapsigargin. In normal neurons, store depletion caused STIM and the IP 3 R to accumulate near the plasma membrane, association of STIM with Orai, clustering of STIM and Orai at ER-plasma-membrane junctions and activation of SOCE. These responses were attenuated in neurons with mutant IP 3 Rs and were rescued by overexpression of STIM with Orai. We conclude that, after depletion of Ca 2+ stores in Drosophila, translocation of the IP 3 R to ER-plasma-membrane junctions facilitates the coupling of STIM to Orai that leads to activation of SOCE.

Mutant IP3 receptors attenuate store-operated Ca2+ entry by destabilizing STIM–Orai interactions in Drosophila neurons