Unique characteristics of Ca2+ homeostasis of the trans-Golgi compartment.

Abstract

Taking advantage of a fluorescent Ca(2+) indicator selectively targeted to the trans-Golgi lumen, we here demonstrate that its Ca(2+) homeostatic mechanisms are distinct from those of the other Golgi subcompartments: (i) Ca(2+) uptake depends exclusively on the activity of the secretory pathway Ca(2+) ATPase1 (SPCA1), whereas the sarco-endoplasmic reticulum Ca(2+) ATPase (SERCA) is excluded; (ii) IP(3) generated by receptor stimulation causes Ca(2+) uptake rather than release; (iii) Ca(2+) release can be triggered by activation of ryanodine receptors in cells endowed with robust expression of the latter channels (e.g., in neonatal cardiac myocyte). Finally, we show that, knocking down the SPCA1, and thus altering the trans-Golgi Ca(2+) content, specific functions associated with this subcompartment, such as sorting of proteins to the plasma membrane through the secretory pathway, and the structure of the entire Golgi apparatus are dramatically altered.