A ferric-chelate reductase for iron uptake from soils

Abstract

Iron deficiency afflicts more than three billion people worldwide, and plants are the principal source of iron in most diets. Low availability of iron often limits plant growth because iron forms insoluble ferric oxides, leaving only a small, organically complexed fraction in soil solutions. The enzyme ferric-chelate reductase is required for most plants to acquire soluble iron. Here we report the isolation of the FRO2 gene, which is expressed in iron-deficient roots of Arabidopsis. FRO2 belongs to a superfamily of flavocytochromes that transport electrons across membranes. It possesses intramembranous binding sites for haem and cytoplasmic binding sites for nucleotide cofactors that donate and transfer electrons. We show that FRO2 is allelic to the frd1 mutations that impair the activity of ferric-chelate reductase. There is a nonsense mutation within the first exon of FRO2 in frd1-1 and a missense mutation within FRO2 in frd1-3. Introduction of functional FRO2 complements the frd1-1 phenotype in transgenic plants. The isolation of FRO2 has implications for the generation of crops with improved nutritional quality and increased growth in iron-deficient soils.

Iron deficiency-mediated stress regulation of four subgroup Ib BHLH genes in Arabidopsis thaliana

“…0 Fe means 0 M Fe plus 50 M ferrozine. Mean values § SD were determined for three to eight measurements tip and in the upper root zones, induced by low iron and down-regulated in Wt loss of function mutants (Eide et al 1996;Robinson et al 1999;Vert et al 2002;Connolly et al 2003;Colangelo and Guerinot 2004;Jakoby et al 2004). FIT was also mainly expressed in roots near the root tip and in the upper root zones, induced by low iron and its promoter was down regulated in Wt loss of function mutants (Colangelo and Guerinot 2004;Jakoby et al 2004;this work).…”

“…To test whether other iron mobilization mutants with chlorotic phenotypes were capable of expressing and upregulating subgroup Ib BHLH genes, we compared gene expression in frd1-1 mutant plants (FRO2 mutant, devoid of iron reductase activity; Robinson et al 1999), irt1-1 mutant plants (devoid of iron transporter activity; Vert et al 2002), and man1 mutant plants (also known as frd3-3, improper iron transport to the shoot; Rogers et al 2002). Generally, these mutant plants were more chlorotic than wild type plants upon iron deWciency.…”

“…This iron mobilization system is strictly regulated. At low iron supply FRO2 and IRT1 genes are induced whereas upon suYcient iron supply the genes are down regulated (Eide et al 1996;Robinson et al 1999;Vert et al 2002). A central transcriptional regulator in this process in tomato is the basic helix-loop-helix (bHLH) factor FER; the A. thaliana ortholog is encoded by the gene FIT (= fer-like iron deWciency-induced transcription factor, previously known as FRU and FIT1, gene number At2 g28160; Bauer et al 2004;Colangelo and Guerinot 2004;Jakoby et al 2004;Yuan et al 2005; FIT was renamed by Bauer, Guerinot and Ling).…”

Genetic engineering in the improvement of plants for phytoremediation of metal polluted soils

“…It belongs to a superfamily of¯avocytochromes, which transport electrons across membranes. FRO2 consists of intramembranous binding sites for heme and cytoplasmic binding sites for NAPDH and FAD cofactors that donate and transfer electrons (Robinson et al, 1999). FRO2 gene was capable of restoring ferric-chelate reductase activity in an Arabidopsis mutant de®cient in this enzyme (frd1) (Robinson et al, 1999).…”

The Arabidopsis Mediator subunit MED16 regulates iron homeostasis by associating with EIN3/EIL1 through subunit MED25

“…In Arabidopsis, ferric reduction oxidase 2 (FRO2) and iron-regulated transporter 1 (IRT1) are two important marker genes for iron uptake. FRO2 encodes a major ferric chelate reductase controlling the amount of iron absorbed from the soil (Robinson et al, 1999;Connolly et al, 2003). IRT1 encodes a member of the ZIP (Zrt/Irt-like Protein) family of proteins used for the transport of Fe 2+ into cells across the plasma membrane (Vert et al, 2002).…”