Abstract

Low phosphate (Pi) availability and high aluminum (Al) toxicity constitute two major plant mineral nutritional stressors that limit plant productivity on acidic soils. Advances toward the identification of genes and signaling networks that are involved in both stresses in model plants such as Arabidopsis thaliana and rice (Oryza sativa), and in other plants as well have revealed that some factors such as organic acids (OAs), cell wall properties, phytohormones, and iron (Fe) homeostasis are interconnected with each other. Moreover, OAs are involved in recruiting of many plant-growth-promoting bacteria that are able to secrete both OAs and phosphatases to increase Pi availability and decrease Al toxicity. In this review paper, we summarize these mutual mechanisms by which plants deal with both Al toxicity and P starvation, with emphasis on OA secretion regulation, plant-growth-promoting bacteria, transcription factors, transporters, hormones, and cell wall-related kinases in the context of root development and root system architecture remodeling that plays a determinant role in improving P use efficiency and Al resistance on acidic soils.

Highlights

  • Publisher’s Note: MDPI stays neutralOccupying over 30% of the world’s arable lands, acid soils encompass a lot of factors constraining plant performance

  • This might be one reason why Al toxicity and P deficiency can independently stimulate the increase of organic acids (OAs) concentrations in plant species that are well adapted to acidic soils [51,52,53]

  • The first transcription factor (TF) that was identified that regulates the expression of ALMT and multidrug and toxic compound extrusion (MATE) was Arabidopsis AtSTOP1 (Sensitive to Proton Rhizotoxicity1)

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Summary

Introduction

Occupying over 30% of the world’s arable lands, acid soils encompass a lot of factors constraining plant performance. CK2 activity inhibition prevented meristem loss that was induced by Pi deficiency, providing evidence that Al toxicity and P deficiency are both related to the cell cycle checkpoint [23] Based on these findings, it is inferred that plants may have evolved some mutual mechanisms to cope with both Al toxicity and P deficiency stresses. The advances in the common mechanisms including the secretion of OAs, plant-growth-promoting bacteria, cell wall properties, phytohormones, and iron (Fe) homeostasis which control Al resistance and P nutrition on acid soils, are summarized, providing insight into the potential solutions to maintain better P status and crop productivity on acid soils by changing root development and root architecture. Root OAs secretion and root development are conserved in response to both Al toxicity and P deficiency

Convergent Evolution of Organic Acids for Plants Adapting to Al Toxicity and
Al-Activated Malate and Citrate Transporters
Regulatory Factors Involved in ALMT1 and MATE1 Expression
Two ABC Transporters Are Involved in Response to P Deficiency and Al Toxicity
Hormone-Mediated Interaction between P Deficiency and Al Stress
Findings
Conclusions and Perspectives
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