Ionomycin is a
calcium ionophore that induces release of
calcium ions (Ca(2+)) from cellular storage to cytoplasm and Ca(2+) influx from the outside of the cell. We investigated the effect of
ionomycin on endoplasmic reticulum (ER)-Golgi transport in the
vesicular stomatitis virus glycoprotein (VSV-G) system.
Ionomycin inhibited transport of VSV-G in a concentration-dependent manner in baby hamster kidney (BHK) cells and HeLa cells. Half-maximum inhibition was observed at 5 μM. The inhibitory effect of
ionomycin was not dependent on the cytoplasmic portion. Chelation of Ca(2+) in culture medium did not affect transport efficiency, but co-incubation with
ionomycin completely shut off transport. These findings highlight the importance of Ca(2+) release from cellular storage. Because the inhibitory effect of
ionomycin was expected to be dependent on mutual interaction of VSV-G and the ER chaperone
calnexin, we further investigated interaction kinetics. In HeLa cells but not BHK cells the interaction of VSV-G and
calnexin was prolonged in the presence of
ionomycin. Taken together, the present results indicate that, by releasing Ca(2+) from cellular storage,
ionomycin inhibits ER-Golgi transport by interfering with the release of VSV-G from
calnexin in HeLa cells. A mechanism of cell type-dependent ER-Golgi transport regulation was revealed.