Upon high Fe supply, organisms tend to use low-affinity Fe transport systems to take up sufficient Fe, while at the same time preventing Fe overload. In contrast, Fe deficiency usually results in the induction of high-affinity Fe transport systems (Andrews et al., 1999; Kaplan, 2002; Van Ho et al., 2002). Depending on the composition and pH of the soil, concentrations of bio-available Fe in the soil can be 104 to 1015 orders of magnitude lower than Fe concentrations met in plant tissues. Obviously, Fe needs to be mobilised in the soil so that adequate amounts can be taken up. It is not clear at this moment whether plants also possess low- and high-affinity transport systems for Fe. Perhaps their growth in soil habitats requires constitutive, high-affinity Fe transport systems.
Two different strategies for Fe mobilisation have been described for plants (Romheld, 1987). Dicotyledonous and non-graminaceous monocotyledonous plants reduce Fe(III) and take up Fe(II). This so-called Strategy I is accompanied by soil acidification and other physiological and morphological reactions, such as secretion of chelators, root hair proliferation and root transfer cell development (recently reviewed by Curie and Briat, 2003; Hell and Stephan, 2003; Schmidt, 2003). Three essential Strategy I components have been characterized that are induced by Fe deficiency. In the absence of the Fe(III) reductase FRO2 or the Fe(II) transporter IRT1, Arabidopsis plants are chlorotic and suffer from Fe deficiency even at normally sufficient Fe supply (Eide et al., 1996; Robinson et al., 1999; Vert et al., 2002). FRO2 and IRT1 genes are induced by Fe deficiency in Arabidopsis (Eide et al., 1996; Robinson et al., 1999; Vert et al., 2003). Their expression is dependent on the regulator gene FRU (= FER-like regulator of iron uptake), encoding a basic helix-loop-helix (bHLH)-type transcription factor (Jakoby et al., 2004). In an independent study, this basic helix-loop-helix gene was identified as an iron regulator and named FIT1 (= Fe-deficiency Induced Transcription Factor 1, Colangelo and Guerinot, 2004). In tomato, a homologous system exists including LeIRTI, LeFROl and the bHLH factor LeFER (Bereczky et al, 2003; Li et al, 2004; Ling et al, 2002). It is therefore likely that the Strategy I system is conserved in dicot species.
Grasses depend on an Fe chelation-based Fe mobilisation mechanism, that involves phytosiderophore production and import of Fe(III)-phyto-siderophore complexes (Strategy II, reviewed by Mori, 1999). The major genes for phytosiderophore production and a phytosiderophore transporter YS1 (= YELLOW STRIPE 1) have been biochemically, genetically or transgenetically analyzed in different grass species [see Curie and Briat (2003), Mori (1999) and reviews in this book for details on the genetic basis for phytosiderophore production; see Curie et al. (2001), Schaaf et al. (2004) and Roberts et al. (2004) for details about maize YS1 ].
Both Strategy I and Strategy II components belong to gene families. The functions of gene family members not involved in root Fe mobilisation are not known. Interestingly, grasses possess homologues of Strategy I genes, and dicot plants contain homologues of some, but not all, Strategy II genes. It is speculated that these additional Strategy I and Strategy II homologues may be involved in Fe transport in organs and tissues other than roots. Such aspects will be further discussed in the following paragraphs.
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