Cross-Talk between Iron Deficiency Response and Defense Establishment in Plants

Abstract

Plants are at risk of attack by various pathogenic organisms. During pathogenesis, microorganisms produce molecules with conserved structures that are recognized by plants that then initiate a defense response. Plants also experience iron deficiency. To address problems caused by iron deficiency, plants use two strategies focused on iron absorption from the rhizosphere. Strategy I is based on rhizosphere acidification and iron reduction, whereas Strategy II is based on iron chelation. Pathogenic defense and iron uptake are not isolated phenomena: the antimicrobial phenols are produced by the plant during defense, chelate and solubilize iron; therefore, the production and secretion of these molecules also increase in response to iron deficiency. In contrast, phytohormone jasmonic acid and salicylic acid that induce pathogen-resistant genes also modulate the expression of genes related to iron uptake. Iron deficiency also induces the expression of defense-related genes. Therefore, in the present review, we address the cross-talk that exists between the defense mechanisms of both Systemic Resistance and Systemic Acquired Resistance pathways and the response to iron deficiency in plants, with particular emphasis on the regulation genetic expression.

Keywords: biotic and abiotic-stress; biotrophic pathogens; iron deficiency in plants; plant immunity; volatile organic compounds.

Figure 1

General view of the plant defense mechanism. During pathogenesis, pathogens produce MAMPs which are recognized by plants through PRR to activate PTI and, consequently, induce ET, ROS, and MAPKs production. On the other hand, there are successful pathogens capable of inhibiting PTI through effectors. Plants respond to effectors through the R gene to activate ETI, which induces ET production and activation of PCD. During PTI, JA/ET and SA activate ISR and SAR resistance paths, respectively. JA/ET regulates transcription factor ERF1 expression, which in turn induces PDF1.2. Additionally, SA regulates NPR1 expression, which in turn induces PR1. Defense genes, PDF1.2 and PR1 are expressed both in the root and plant shoot.

Figure 2

Strategies used by plants for iron uptake. In iron deficiency conditions, Strategy I plants activate proton secretion through AHA for rhizosphere acidification. This mechanism is accompanied by phenol release, which chelates iron. Subsequently, free or chelated iron is reduced by ferric chelate reductase FRO2 and internalized by IRT1. This mechanism is regulated by the transcription factors PYE, bHLH34/38/39/100/101/104/105, and the ubiquitin ligase BTS. In Strategy II plants, phytosiderophores which chelate iron are secreted through TOM1. The chelated iron is internalized by YS1. The Strategy II mechanism is regulated by the transcription factors IRO2/IRO3, IDEF1, and the ubiquitin ligase HRZ1.

Figure 3

Cross-talk between iron and defense responses. During iron deficiency, plants induce ET, JA, and SA synthesis, and other phytohormones that regulate defense responses in plants. In turn, ET and JA regulates iron uptake by an induction in the expression of ERF1 and MYC2 (in the shoot) [53], respectively. These genes encode transcription factors that activate of the defense gene PDF1.2 (ISR pathway) and the FIT gene, a transcriptional regulator of the iron deficiency response pathway (in the shoot). The response is similar when the plant is attacked by a pathogen. During pathogenesis, the plant produces, in addition to phenols, phytohormones such as ET, JA and SA. The SA activate the SAR defense pathway by inducing the expression of the PR1 gene through NPR1, which encode a transcription factor. SA also induces the expression of the bHLH38 gene that participates in the regulation of the response to iron deficiency pathway. Therefore, when plants perceive iron deficiency, the response machinery to this pathway is activated, through the induction of the expression of genes such as PYE, BTS, ILR3, bHLH34/38/39/100/101/104 and FIT [54], in addition to the secretion of phenols through the protein encoded by PDR9, which facilitate iron chelation. On the other hand, during iron deficiency response, defense mechanisms are activated to protect plants from pathogens.