Deconstructing iron-deficiency signaling pathways in plants

Our research has revealed distinct signaling pathways in the model plant Arabidopsis that control iron-deficiency responses and further highlights the complexity of the networks driving plant responses to low iron nutrition. Understanding how plants deal with iron deficiency is critical to human nutrition because vegetarian diets based on iron deprived crops may enforce anemia.

HFSP Career Development Award holder Gregory Vert and colleagues
authored on Thu, 29 November 2012

Understanding iron-deficiency responses in plants is necessary for the creation or cultivation of food sources enriched in iron and other nutrients. Iron is vital for basic biological processes such as respiration and photosynthesis. Iron serves as an electron donor and acceptor in the enzymatic reactions that drive biological energy generation. However, this same reactivity of iron makes it toxic at high concentrations. The availability and distribution of iron within an organism is thus subjected to tight control. Although iron is extremely ubiquitous in soils, it is not readily available for plant metabolism. Rather it exists as insoluble iron oxides in most soils and can be a limited nutrient in calcareous soils like those found across much of Europe. Arabidopsis mobilizes soil iron by excreting acids to solubilize the iron-soil particles. The soluble ferric iron is then reduced to ferrous iron, which can then be transported across the root outer membrane to use in growth and development.

Figure: Model representing the complexity of plant responses to low iron availability in the soil. FIT controls the expression of root genes involved in iron uptake, among others, by direct binding to heir promoters. bHLH100 and bHLH101 are acting in a different network, promoting the expression of a different subset of genes under iron starvation.

This process of iron uptake has been shown to be genetically controlled by a basic helix-loop-helix (bHLH) transcription factor called FIT, proposed early on to be a master regulator of iron-deficiency responses (Ref 1). The current work investigated the direct and indirect target genes of FIT to shed light on the networks controlling plant responses to iron starvation. This work demonstrated that many genes regulated by low iron in roots, including genes encoding the iron uptake machinery, were directly controlled by FIT by direct binding and activation of transcription. We also uncovered that additional factors, whose identity is not yet known, are working together with FIT to promote activation of iron-regulated genes.

In order to elucidate the intricate mechanisms driving iron-deficiency responses, we further examined the role of two other bHLH transcription factors regulated by iron starvation, named bHLH100 and bHLH101. A mutant plant lacking both of these transcription factors showed severe chlorosis, a hallmark of iron deficiency. A genome-wide transcriptomic analysis of such double mutant plants surprisingly revealed that the FIT-network was unaffected, thus pointing to the existence of a new network critical for plant survival when the availability of iron is low and controlled by both factors. bHLH100 and bHLH101 appear to be important in directing either the remobilization of iron stores under conditions of iron deficiency or in regulating metabolic changes to cope with low-iron conditions.

To summarize, this work helps to deconstruct the complicated networks that together allow a plant to cope with soils with low iron availability. In addition, this work opens new areas in trying to manipulate iron homeostasis in plants.

Reference

Arabidopsis bHLH100 and bHLH101 control iron homeostasis via a FIT-independent pathway. Sivitz AB, Hermand V, Curie C, Vert G. PLoS One. 2012;7(9):e44843. doi: 10.1371/journal.pone.0044843. Epub 2012 Sep 11.PMID:22984573 [PubMed - in process]

Other references

Ref 1: The essential bHLH protein FIT1 is required for the iron deficiency response. Colangelo EP, Guerinot ML. (2004)  Plant Cell 16: 3400-3412.

Pubmed link