Abstract
BackgroundUnder limited iron (Fe) availability maize, a Strategy II plant, improves Fe acquisition through the release of phytosiderophores (PS) into the rhizosphere and the subsequent uptake of Fe-PS complexes into root cells. Occurrence of Strategy-I-like components and interactions with phosphorous (P) nutrition has been hypothesized based on molecular and physiological studies in grasses.ResultsIn this report transcriptomic analysis (NimbleGen microarray) of Fe deficiency response revealed that maize roots modulated the expression levels of 724 genes (508 up- and 216 down-regulated, respectively). As expected, roots of Fe-deficient maize plants overexpressed genes involved in the synthesis and release of 2’-deoxymugineic acid (the main PS released by maize roots). A strong modulation of genes involved in regulatory aspects, Fe translocation, root morphological modification, primary metabolic pathways and hormonal metabolism was induced by the nutritional stress. Genes encoding transporters for Fe2+ (ZmNRAMP1) and P (ZmPHT1;7 and ZmPHO1) were also up-regulated under Fe deficiency.Fe-deficient maize plants accumulated higher amounts of P than the Fe-sufficient ones, both in roots and shoots. The supply of 1 μM 59Fe, as soluble (Fe-Citrate and Fe-PS) or sparingly soluble (Ferrihydrite) sources to deficient plants, caused a rapid down-regulation of genes coding for PS and Fe(III)-PS transport, as well as of ZmNRAMP1 and ZmPHT1;7.Levels of 32P absorption essentially followed the rates of 59Fe uptake in Fe-deficient plants during Fe resupply, suggesting that P accumulation might be regulated by Fe uptake in maize plants.ConclusionsThe transcriptional response to Fe-deficiency in maize roots confirmed the modulation of known genes involved in the Strategy II and revealed the presence of Strategy I components usually described in dicots. Moreover, data here presented provide evidence of a close relationship between two essential nutrients for plants, Fe and P, and highlight a key role played by Fe and P transporters to preserve the homeostasis of these two nutrients in maize plants.
Highlights
Under limited iron (Fe) availability maize, a Strategy II plant, improves Fe acquisition through the release of phytosiderophores (PS) into the rhizosphere and the subsequent uptake of Fe-PS complexes into root cells
Root transcriptomic response to Fe deficiency In order to investigate the Fe-deficient response in maize, microarray analyses were performed on samples of Fe-deficient and Fe-sufficient roots
In a recent study Nozoye et al [8] suggested the involvement of ZmNRAMP1 (GRMZM2G178190) in the acquisition of external ferrous ions, as already reported for the rice homologous OsNRAMP1 and OsNRAMP5 [12,13,14]. Consistent with this assumption, we found the induction of ZmNRAMP1 in Fe-deficient maize roots; gene expression was down-regulated by the treatment with the three Fe-sources with a pattern reflecting the amount of 59Fe-Citrate or (59Fe) taken up by deficient plants
Summary
Under limited iron (Fe) availability maize, a Strategy II plant, improves Fe acquisition through the release of phytosiderophores (PS) into the rhizosphere and the subsequent uptake of Fe-PS complexes into root cells. The level of plant-available Fe in the soil solution is determined by a variety of natural ligands (such as microbial siderophores, humic substances and root exudates) which are able to mobilize Fe from oxides/hydroxides form to Fe(III) chelates [3] and can be used by plants directly or through reduction-based mechanisms. Strategy I is used by all dicots and non‐graminaceous monocots, that respond to Fe‐deficiency by releasing in the rhizosphere protons and chelating/reducing agents (as carboxylates and phenolic compounds) to mobilize Fe from sparingly soluble forms. Afterwards, a ferric-chelate reductase at the surface of root cells (FRO) mediates the reduction of ferric ions to ferrous form [4, 5]. The ferrous ion is, in turn, acquired by roots through a Fe2+ transporter belonging to the ZIP metal transporter family (iron regulated metal transporter, IRT) [6]
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