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

Taking advantage of a fluorescent Ca²⁺ indicator selectively targeted to the trans-Golgi lumen, we here demonstrate that its Ca²⁺ homeostatic mechanisms are distinct from those of the other Golgi subcompartments: (i) Ca²⁺ uptake depends exclusively on the activity of the secretory pathway Ca²⁺ ATPase1 (SPCA1), whereas the sarco-endoplasmic reticulum Ca²⁺ ATPase (SERCA) is excluded; (ii) IP₃ generated by receptor stimulation causes Ca²⁺ uptake rather than release; (iii) Ca²⁺ 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 Ca²⁺ 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.