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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: Traffic. 2014 Oct 27;15(12):1344–1365. doi: 10.1111/tra.12229

Figure 10. Summary of results.

Figure 10

A) When Cu levels are low, about 80% of ATP7B resides in the TGN, with the remainder in small vesicles that localize near substrate side of the cell, close to the coverslip. Treatment of WIF-B cells with Baf in low Cu does not perturb localization in the TGN. B) When Cu levels are increased, this induces a rapid doubling of ATP7B vesicles, presumably derived from the TGN. These vesicles transiently traverse a pool of large EEA1-positive endosomes located near the substrate. Segregation and exit from these “basal” endosomes is inhibited by loss of luminal acidification. A second site of Baf action was revealed to be rapid recycling through an endosomal pool that lies in close association with the apical plasma membrane. Treatment with Baf promotes accumulation in these endosomes. C) When Cu is removed to induce ATP7B trafficking back to the TGN, the process proceeds similarly in the absence or presence of Baf. Thus the role of acidification is selective for ATP7B trafficking routes induced by Cu.