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Abstract:
Evidence suggests that GTP but not GTPγS activates Ca2+ movement between myo-inositol 1,4,5-trisphoshate (IP3)-sensitive and -insensitive Ca2+ pools (1). Measuring 45Ca2+ uptake into pancreatic microsomal vesicles we have determined the sizes of three different Ca2+ pools which release Ca2+ in response 1) to IP3, 2) to caffeine, and 3) to both IP3 and caffeine (“common” Ca2+ pool). In the presence of GTP the size of the IP3-sensitive Ca2+ pool is decreased whereas the “common” Ca2+ pool is increased as compared to control Ca2+ pool sizes in the presence of GTPγS. This effect of GTP is inhibited by bafilomycin B1, a specific inhibitor of vacuolar type H+ ATPases (2). We conclude that GTP induced connection between IP3 and caffeine-sensitive Ca2+ pools is triggered by intravesicular acidification and involves function of small GTP-binding proteins, known to mediate interorganelle transfer.
