Abstract

Relatively little is known about how metals such as iron are effluxed from cells, a necessary step for transport from the root to the shoot. Ferroportin (FPN) is the sole iron efflux transporter identified to date in animals, and there are two closely related orthologs in Arabidopsis thaliana, IRON REGULATED1 (IREG1/FPN1) and IREG2/FPN2. FPN1 localizes to the plasma membrane and is expressed in the stele, suggesting a role in vascular loading; FPN2 localizes to the vacuole and is expressed in the two outermost layers of the root in response to iron deficiency, suggesting a role in buffering metal influx. Consistent with these roles, fpn2 has a diminished iron deficiency response, whereas fpn1 fpn2 has an elevated iron deficiency response. Ferroportins also play a role in cobalt homeostasis; a survey of Arabidopsis accessions for ionomic phenotypes showed that truncation of FPN2 results in elevated shoot cobalt levels and leads to increased sensitivity to the metal. Conversely, loss of FPN1 abolishes shoot cobalt accumulation, even in the cobalt accumulating mutant frd3. Consequently, in the fpn1 fpn2 double mutant, cobalt cannot move to the shoot via FPN1 and is not sequestered in the root vacuoles via FPN2; instead, cobalt likely accumulates in the root cytoplasm causing fpn1 fpn2 to be even more sensitive to cobalt than fpn2 mutants.

Highlights

  • Iron is essential for plant growth, yet the redox properties that make iron biologically useful make free iron highly destructive

  • Data are presented as a scaled pool hybridization difference (SPHD), representing the difference between the hybridization of the two pools at the single feature polymorphisms (SFPs), scaled so that a pure Col-0 pool would be at 1 and a pure Ts-1 pool would be at À1

  • Combined with the shoot inductively coupled plasma–mass spectrometry (ICP-MS) data, this indicates that without FPN2, cobalt is not sequestered in the root vacuoles, allowing its movement to the shoot, resulting in sensitivity to cobalt

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Summary

Introduction

Iron is essential for plant growth, yet the redox properties that make iron biologically useful make free iron highly destructive. FPN2 was previously reported to be expressed in the roots of iron-deficient plants (Colangelo and Guerinot, 2004) and to localize to the vacuolar membrane (Schaaf et al, 2006). Upregulated in response to iron deficiency, FPN2 was reported to function in nickel sequestration (Schaaf et al, 2006). As nickel is one of the divalent cations taken up by IRT1, this suggests that plants have strategies to deal with the influx of potentially toxic metals that enter the root during iron deficiency. A similar role has been described for MTP3, which is iron regulated, localizes to the vacuolar membrane, and is thought to sequester zinc in the vacuole during iron deficiency (Arrivault et al, 2006)

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