Abstract

Stylo has a great potential for Al3+ resistance in acidic soils through secretion of citrate from the roots. To get insight into the molecular mechanisms responsible, transcriptomic changes were investigated in the roots after treatment with T01 (−Al3+, pH6.0), T02 (−Al3+, pH4.3) and T03 (50 µM AlCl3, pH4.3). In total, 83,197 unigenes generated from 130,933 contigs were obtained. Of them, 282, 148 and 816 differentially expressed unigenes (DEGs) were revealed in T01_vs_T02, T02_vs_T03 and T01_vs_T03 comparison, respectively (FDR < 0.001, log2FC > 2). DEGs by Al3+ were related to G-proteins, diacyglycerol and inositol metabolism, calcium-signaling, transcription regulation, protein modification and transporters for detoxification of Al3+. Additionally, Al3+ facilitates citrate synthesis via modifying gene expression of pathways responsible for citrate metabolism. Overall, Al3+ resistance in stylo involves multiple strategies and enhancement of citrate anabolism. The Al3+ signal transmits through heterotrimeric G-proteins, phospholipase C, inositol triphosphate, diacylglycerol, Ca2+ and protein kinases, thereby activating transcription and anion channels in plasma membrane, and resulting in citrate secretion from stylo roots.

Highlights

  • Trivalent aluminum (Al3+) toxicity is a major constraint for root growth and crop yields of plants in acidic soils, which constitute 50% of the potentially arable lands worldwide[1]

  • The first class of resistance genes encoding malate and citrate efflux transporters (ALMTs) has been identified in wheat, Arabidopsis, rape and rye[2]. Another protein family involved in Al3+ tolerance is from multidrug and toxic compound extrusion proteins (MATEs) that are associated with Al3+-activated citrate exudation in plant species[2]

  • The largest quantity of citrate exudation was detected at 24 h after 50 μM AlCl3 treatment with no more than a 25% inhibition of relative root growth (RRG) compared to the control (−Al3+) (Fig. 1A,B)

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Summary

Introduction

Trivalent aluminum (Al3+) toxicity is a major constraint for root growth and crop yields of plants in acidic soils, which constitute 50% of the potentially arable lands worldwide[1]. The first class of resistance genes encoding malate and citrate efflux transporters (ALMTs) has been identified in wheat, Arabidopsis, rape and rye[2]. Another protein family involved in Al3+ tolerance is from multidrug and toxic compound extrusion proteins (MATEs) that are associated with Al3+-activated citrate exudation in plant species[2]. Subsequent studies have identified sensitive to proton rhizotoxicity 1 (STOP1) in Arabidopsis and Al3+ resistance transcription factor 1 (ART1) in rice as transcription factors that regulate expression of a suite of Al3+-resistance genes[5,6] Despite of these findings, the mechanisms that modulate gene expression responsible for Al3+-induced secretion of citrate remain unclear. The aim was to characterize the pathways that orchestrate expression of genes responsible for Al3+-induced secretion of citrate in stylo

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