The uptake, translocation and compartmentalization of Fe are essential for plant cell function and life cycle. Despite rapid progress in our understanding of Fe homeostasis in plants, Fe transport from the cytoplasm to mitochondria was, until recently, poorly understood. The screening of 3,993 mutant lines for symptoms of Fe deficiency resulted in the identification and characterization of a major mitochondrial Fe transporter (MIT) in rice. MIT was found to localize to mitochondria and to complement the growth of a yeast strain defective in mitochondrial Fe transport. The knockout of MIT resulted in a lethal phenotype, and in knock-down plants, several agronomic characteristics were compromised, such as plant height, average number of tillers, days to flower, fertility and yield. Changes in the expression of genes involved in Fe transport suggested a disturbance of cellular Fe transport. Furthermore, the mitochondrial Fe concentration and the activity of the mitochondrial Fe-S enzyme aconitase were significantly reduced compared with wild-type plants. The identification of MIT is a significant advance in the field of plant Fe nutrition and should facilitate the cloning of paralogs from other plant species.
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