Baseline cytosolic Ca2+ oscillations derived from a non-endoplasmic reticulum Ca2+ store

Cytosolic Ca2+ oscillations can be due to cycles of release and re-uptake of internally stored Ca2+. To investigate the nature of these Ca2+ stores, we expressed the Pmr1 Ca2+ pump of Caenorhabditis elegans in COS-1 cells and pretreated the cells with thapsigargin to prevent Ca2+ uptake by the sarco(endo)plasmic reticulum Ca2+-ATPase. Pmr1 co-localized with the Golgi-specific 58K protein and was targeted to a Ca2+ store that was less leaky for Ca2+ than the endoplasmic reticulum and whose inositol trisphosphate receptors were less sensitive to inositol trisphosphate and ATP than those in the endoplasmic reticulum. ATP-stimulated Pmr1-overexpressing cells responded after a latency to extracellular Ca2+ with a regenerative Ca2+ signal, which could be prevented by caffeine. They also produced very stable ilimaquinone-sensitive baseline Ca2+ spikes, even in the presence of thapsigargin. Such responses never occurred in non-transfected cells or in cells that overexpressed the type-1 sarco(endo)plasmic reticulum Ca(2+-)ATPase. Abortive Ca2+ spikes also occurred in histamine-stimulated untransfected HeLa cells pretreated with thapsigargin, and they too were inhibited by ilimaquinone. We conclude that the Pmr1-induced Ca2+ store, which probably corresponds to the Golgi compartment, can play a crucial role in setting up baseline Ca2+ spiking.