Date of Award


Document Type

Open Access Dissertation


Biological Sciences

First Advisor

Erin Connolly


Iron (Fe) is the fourth most abundant element in the Earth’s crust, yet the availability of Fe to plants is often limited. This is because in most soil types, Fe precipitates as ferric-oxyhydroxy complexes, making it unavailable for uptake by plants. While the mechanisms involved in Fe uptake from the soil are relatively well understood, the mechanisms involved in its further distribution to the aerial portion of the plant and to subcellular compartments are not fully understood. During Fe deprivation, plants up-regulate root Fe acquisition machinery. How plants sense Fe deprivation and tie the Fe status of the plant to appropriate rates of root Fe uptake, is not well understood. Chloroplasts and mitochondria represent significant Fe sinks in plants and it is assumed that plants monitor the Fe status of these two compartments; if chloroplasts or mitochondria sense Fe limitation, a long distance signal is generated, which serves to upregulate the root Fe acquisition machinery. A number of enzymes involved in the process of energy production in mitochondria are dependent on Fe either as Fe-S clusters or heme cofactors. Thus adequate import of Fe to the mitochondria is vital for the function of this organelle, which becomes all the more essential during Fe starvation. Despite this, not much is known about the Fe trafficking to/from mitochondria. In this study, I describe the mechanisms involved in mitochondrial iron acquisition from the cytoplasm in plants. Two types of proteins, a ferric chelate reductase (FRO3) and two functionally redundant transporters (MIT1 and MIT2 for Mitochondrial Iron Transporter) mediate Fe uptake by mitochondria. In the absence of either FRO3 or MIT1/MIT2, total Fe content of the mitochondria is reduced and the plants exhibit signature Fe deficiency phenotypes. Furthermore, while it is presumed that MITs are localized to the mitochondrial inner membrane, our membrane topology studies place FRO3 on the outer mitochondrial membrane with its catalytic site facing the inter membrane space of the organelle. Thus we believe that FRO3 and MITs work together during Fe deprivation to reduce and shuttle the ferric iron pools of the IMS to the matrix to meet mitochondrial Fe requirements. Additionally, we found that, while FRO3 is absolutely essential for seed production during Fe deprivation, loss of MIT1 and MIT2 leads to embryo lethality. In this study, we show that FRO3 and the MITs are essential for mitochondrial Fe homeostasis and thus for proper growth and development of the plant.

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