It 2009). Secretion of secondary metabolites can positively

It is evident that nutrient uptake in plants needs to
be fine-tuned to counteract nutrient deficiency but also overaccumulation and
hence toxicity. To date, two Fe uptake strategies have been investigated,
concerning the uptake from the soil into epidermal cells. All plants except the
Poaceae execute a Fe3+ reduction-based
uptake strategy (Strategy I). Poaceae,
however, excrete non-proteinogenic amino acids, phytosiderophores, to complex
Fe3+ (Strategy II) (Marschner et al., 1986; Romheld and Marschner, 1986).

 

1.1.1       
Reduction-based
Fe Uptake (Strategy I)

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The Fe uptake strategy employed by all
non-graminaceous plants, such as Arabidopsis
thaliana, consists of three steps that are executed by Fe-responsive, plasma-membrane
localized proteins, located in epidermal root cells (Figure 1).

Soil acidification allows solubilizing Fe3+
which is bound to negatively charged soil particles (Step 1) (Marschner et al., 1986). Several Arabidopsis ATPases were
shown to be responsive to Fe limitations, but one promising candidate was Arabidopsis
H(+)-ATPASE2 (AHA2). aha2 knock-out mutants displayed a
significant reduction in net proton flux compared to WT when grown under sufficient and deficient Fe conditions, confirming
a major role of AHA2 in rhizosphere acidification (Santi and Schmidt, 2009).

Secretion of secondary metabolites can positively
affect the Fe uptake response. As seen in red clover, secreted phenolic
compounds enhance the utilization of apoplastic Fe3+ (Jin et al., 2007). Similarly, the expression of
respective efflux transporter and the presence of phenolic compounds support
the Fe uptake under limited conditions in Arabidopsis. FERULOYL-COA 6′-HYDROXYLASE
1 (F6’H1), a player in the phenylpropanoid biosynthesis
pathway, as well as the phenolic transporter PLEIOTROPIC DRUG RESISTANCE9 (PDR9) (also called ABCG37) are key players in Arabidopsis. Generally,
the secretion of phenolic compounds and expression of ABCG37 are upregulated under Fe deficiency. Thus, it is believed
that the secretion of different phenolic compounds, such as coumarins, enhances
the Fe3+ assimilation and mobilization. In Arabidopsis,
especially the coumarin scopoletin seems to play an important role (Rodriguez-Celma et
al., 2013; Fourcroy et al., 2014; Schmid et al., 2014; Schmidt et al., 2014;
Fourcroy et al., 2016).

Once Fe3+ is available, it is subsequently
reduced to Fe2+ by FERRIC REDUCTASE-OXIDASE 2 (FRO2) (Robinson et al., 1999). FRO2 was identified based on its
sequence similarity to yeast ferric-chelate reductases and the human phagocytic
NADPH oxidase (Robinson et al., 1999). The respective loss-of-function
mutant frd1 shows decreased Fe chelate
reductase activity (Yi and Guerinot, 1996). When grown under Fe deficient
conditions, the frd1 mutant phenotype,
such as severe leaf chlorosis, could be complemented by FRO2 expression. Overexpression of FRO2 even enhanced tolerance to Fe deficiency (Robinson et al., 1999; Connolly et al., 2003) (Step
2).

In the last step, Fe2+
is transported across the membrane from the rhizosphere into epidermal cells. In
a yeast -complementation assay, IRON REGULATED TRANSPORTER1 (IRT1) was able to
rescue the growth defect of the Fe uptake mutant strain fet3/fet4 under limited Fe supply (Eide et al., 1996). irt1-1 knock-out mutants display severe
Fe deficiency chlorosis, growth defects, disturbed photosynthetic capacity
under Fe deficient conditions as well as reduced leaf Fe content when grown in
soil. Hence, IRT1 is responsible for the Fe uptake in plants.  Interestingly, IRT1 is not highly selective,
since it also transports other divalent metals in the plant (Henriques et al., 2002; Varotto et al., 2002; Vert et
al., 2002).

The question remained which upstream located regulator
coordinates those processes and hence fine-tunes the action of the respective proteins,
involved in Strategy I. The basic helix-loop-helix (bHLH) transcription factor
FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR (FIT, bHLH029), belonging
to subgroup IIIa within the A. thaliana bHLH family (Heim et al., 2003), was
shown to execute this task. Upon dimerization with bHLH subgroup Ib proteins, bHLH038,
bHLH039, bHLH100 and bHLH101, which are upregulated by Fe deficiency
independently from FIT, FIT induces the expression of AHA2, FRO2 and IRT1 upon Fe limitation (Heim et al., 2003; Colangelo and Guerinot, 2004;
Jakoby et al., 2004; Yuan et al., 2005; Vorwieger et al., 2007; Wang et al.,
2007; Yuan et al., 2008; Ivanov et al., 2012; Wang et al., 2013; Mai et al.,
2015; Mai et al., 2016; Naranjo-Arcos et al., 2017).

The question remained which upstream located regulator
coordinates those processes and hence fine-tunes the action of the respective proteins,
involved in Strategy I. The basic helix-loop-helix (bHLH) transcription factor
FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR (FIT, bHLH029), belonging
to subgroup IIIa within the A. thaliana bHLH family (Heim et al., 2003), was
shown to execute this task. Upon dimerization with bHLH subgroup Ib proteins, bHLH038,
bHLH039, bHLH100 and bHLH101, which are upregulated by Fe deficiency
independently from FIT, FIT induces the expression of AHA2, FRO2 and IRT1 upon Fe limitation (Heim et al., 2003; Colangelo and Guerinot, 2004;
Jakoby et al., 2004; Yuan et al., 2005; Vorwieger et al., 2007; Wang et al.,
2007; Yuan et al., 2008; Ivanov et al., 2012; Wang et al., 2013; Mai et al.,
2015; Mai et al., 2016; Naranjo-Arcos et al., 2017).