Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.15.203646v1?rss=1 Authors: Kim, L. J., Tsuyuki, K. M., Hu, F., Park, E. Y., Zhang, J., Gallegoe Iraheta, J., Chia, J.-C., Huang, R., Tucker, A. E., Clyne, M., Castellano, C., Kim, A., Chung, D. D., DaVeiga, C. T., Parsons, E. M., Vatamaniuk, O. K., Jeong, J. Abstract: Mitochondria and chloroplasts are organelles with high iron demand that are highly susceptible to iron-induced oxidative stress. Despite the necessity of strict iron regulation in these organelles, much remains unknown about mitochondrial and chloroplast iron transport in plants. Here, we show that Arabidopsis Ferroportin 3 (FPN3) is an iron exporter dual-targeted to mitochondria and chloroplasts. FPN3 is expressed in shoots regardless of iron conditions, but is iron-regulated in the roots. fpn3 mutants cannot grow as well as wild type under iron-deficient conditions and shoot iron levels are reduced in fpn3 mutants compared to wild type. Analyses of iron homeostasis gene expression in fpn3 mutants and ICP-MS measurements suggest that iron levels in the mitochondria and chloroplasts are increased relative to wild type, consistent with the proposed role of FPN3 as a mitochondrial/plastid iron exporter. In iron deficient fpn3 mutants, abnormal mitochondrial ultrastructure was observed, whereas chloroplast ultrastructure was not affected, implying that FPN3 plays a critical role in iron metabolism in mitochondria. Overall, we propose that FPN3 is crucial for iron homeostasis. One sentence summaryFPN3 is an iron exporter dual-targeted to the mitochondria and plastids and is required for optimal growth under iron deficiency. Copy rights belong to original authors. Visit the link for more info