Regulation of phytosiderophore release and antioxidant defense in roots driven by shoot-based auxin signaling confers iron toxicity tolerance in wheat

Abstract

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Iron (Fe) is essential but harmful for plants at toxic level; however, how wheat tolerates excess Fe remains vague. This study aims to elucidate the mechanisms underlying Fe toxicity tolerance and signaling in wheat. Fe toxicity caused morpho-physiological retardation in BR 26 (sensitive) but not in BR 27 (tolerant). Phytosiderophore and 2-deoxymugineic acid showed no changes in BR 27 but significantly increased in BR 26 due to Fe toxicity. Further, expression of TaSAMS, TaDMAS1 and TaYSL15 significantly downregulated in BR 27 roots, while these were upregulated in BR 26. It confirms that inhibition of phytosiderophore directs less Fe accumulation in BR 27. However, phytochelatin and expression of TaPCS1 and TaMT1 showed no significant induction under Fe toxicity. Additionally, excess Fe showed increased CAT, POD and GR along with glutathione, cysteine and proline in roots in BR 27. Interestingly, BR 27 self-grafts and plants having BR 26 rootstock attached to BR 27 scion had no Fe-toxicity induced adverse effect on morphology but showed BR 27 type expressions, confirming that shoot-derived signal triggering Fe-toxicity tolerance in roots. Finally, auxin inhibitor applied with Fe toxicity caused significant decline in morpho-physiological parameters along with increased TaSAMS and TaDMAS1 expression in roots of BR 27, revealing the involvement of auxin signaling with Fe-toxicity tolerance. These findings propose that Fe-toxicity tolerance in wheat is attributed to the regulation of phytosiderophore limiting Fe acquisition along with increased antioxidant defense in roots driven by shoot-derived auxin signaling.

Keywords

• auxin signaling
• wheat
• Fe toxicity
• Phytosiderophore release
• Reciprocal grafting
• 2-DMA.