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. 2014 Apr 10;9:e28787. doi: 10.4161/psb.28787

graphic file with name psb-9-e28787-g1.jpg

Figure 1. Role of SNX proteins in IRT1 trafficking and stability. (A) In wild type, under iron deficiency the newly synthesized IRT1 protein follows the secretory pathway and, passing through the early endosomes, enters the PM where it imports bivalent iron from the root apoplast. From the PM IRT1 is internalized and sent through the early endosome to the sorting endosome, where a decision needs to be made. IRT1 is either targeted for degradation (red punctate arrows) through the late endosome, or travels back to the early endosome in a SNX-dependent manner, to be sent again to the PM. (B) In the absence of SNX proteins, IRT1 molecules cannot exit the sorting endosome and are degraded (red-and-black arrows). Only the newly-synthesized IRT1 molecules can reach the PM. As a consequence of the lower number of transporters at the PM, reduced amounts of iron are imported into the cell.