Abstract

Depletion of Ca 2+ stores in Xenopus oocytes activated entry of Ca 2+ across the plasma membrane, which was measured as a current I SOC in subsequently formed cell-attached patches. I SOC survived excision into inside-out configuration. If cell-attached patches were formed before store depletion, I SOC was activated outside but not inside the patches. I SOC was potentiated by microinjection of Clostridium C3 transferase, which inhibits Rho GTPase, whereas I SOC was inhibited by expression of wild-type or constitutively active Rho. Activation of I SOC was also inhibited by botulinum neurotoxin A and dominant-negative mutants of SNAP-25 but was unaffected by brefeldin A. These results suggest that oocyte I SOC is dependent not on aqueous diffusible messengers but on SNAP-25, probably via exocytosis of membrane channels or regulatory molecules.

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