Aluminum (Al) rhizotoxicity in acidic soils (at pH<5.5, Al3+ is the predominant phytotoxic species) is a major environmental constraint limiting food production worldwide. Al is cytotoxic and genotoxic (binds with DNA) and inhibits root growth at very low concentrations. Al binds to and disturbs key molecules at the apoplast and plasma membrane (PM) surface, including certain polysaccharides in the cell wall, and phospholipids and H+-ATPases at the PM, causing Al damage in several biological processes. By contrast, Al generates ROS inside cells, which results in cellular damage, and eventually cell death. To circumvent such sequential Al toxicity, plants initiate diverse Al resistance mechanisms. Molecular mechanisms underlying Al-inducible and -activated resistance have been studied extensively during the last decade. These studies provide unique insights into Al-resistance and raise new questions regarding how plants manage these responses with other biological processes.
Al-activated/inducible mechanisms play critical roles in Al resistance. These have been identified in the malate excretion process mediated by ALMT1 (ALUMINUM ACTIVATED MALATE TRANSPORTER1), which results in detoxification of Al3+ at the rhizosphere. Attraction of Al3+ to the PM and binding to ALMT1 immediately activates its malate transport capacity while simultaneously triggering an increase in ALMT1gene expression at very low concentrations. In Arabidopsis, these Al-dependent responses are regulated by a complex network involving activation of specific signaling pathways (protein phosphorylation, phosphoinositide signaling, calcium-signaling) and transcription factors (TFs). Recent studies revealed that posttranslational regulation of a critical TF, SENSITIVE TO PROTON RHIZOTOXICITY 1 (STOP1), is involved in the Al-inducible ALMT1-expression. Other studies on Arabidopsis STOP1 identified its pleiotropic roles in stress tolerance. Hypoxia tolerance in the shoots and Al, H+, and low P tolerance is positively regulated by STOP1; in contrast, drought tolerance is negatively regulated by STOP1 via modulation of K+-uptake. It indicates that Al tolerance is regulated both specifically and together with other stress tolerances. In this Research Topic, we would like to understand such complex systems at molecular levels, including identification of molecules involved in Al-signaling such as sensor and regulatory proteins and TFs.
This Research Topic will focus on understanding the molecular mechanisms underlying the signaling cascades involved in Al resistance responses in model plant species as well as crop species. As described, these processes are regulated by a complex network, including crosstalk with other signaling pathways and early and late responses. Identification of such regulatory processes by genetics (including GWAS and chemical genetics), multi-omics, and bioinformatics-based approaches are welcome. Molecular physiological studies focusing on \understanding crosstalk and pleiotropic effects by Al-signaling are also welcome.
• Genetic studies identifying Al signal
• Comparative genomics and molecular physiology of Al tolerance (e.g. studies of STOP1-system in crops)
• Pleiotropy of Al-inducible Al tolerance.
• Novel Al inducible Al resistant mechanisms
Please note descriptive studies that report responses of growth, yield, or quality to Al stress will not be considered if they do not progress physiological understanding of these responses.
Aluminum (Al) rhizotoxicity in acidic soils (at pH<5.5, Al3+ is the predominant phytotoxic species) is a major environmental constraint limiting food production worldwide. Al is cytotoxic and genotoxic (binds with DNA) and inhibits root growth at very low concentrations. Al binds to and disturbs key molecules at the apoplast and plasma membrane (PM) surface, including certain polysaccharides in the cell wall, and phospholipids and H+-ATPases at the PM, causing Al damage in several biological processes. By contrast, Al generates ROS inside cells, which results in cellular damage, and eventually cell death. To circumvent such sequential Al toxicity, plants initiate diverse Al resistance mechanisms. Molecular mechanisms underlying Al-inducible and -activated resistance have been studied extensively during the last decade. These studies provide unique insights into Al-resistance and raise new questions regarding how plants manage these responses with other biological processes.
Al-activated/inducible mechanisms play critical roles in Al resistance. These have been identified in the malate excretion process mediated by ALMT1 (ALUMINUM ACTIVATED MALATE TRANSPORTER1), which results in detoxification of Al3+ at the rhizosphere. Attraction of Al3+ to the PM and binding to ALMT1 immediately activates its malate transport capacity while simultaneously triggering an increase in ALMT1gene expression at very low concentrations. In Arabidopsis, these Al-dependent responses are regulated by a complex network involving activation of specific signaling pathways (protein phosphorylation, phosphoinositide signaling, calcium-signaling) and transcription factors (TFs). Recent studies revealed that posttranslational regulation of a critical TF, SENSITIVE TO PROTON RHIZOTOXICITY 1 (STOP1), is involved in the Al-inducible ALMT1-expression. Other studies on Arabidopsis STOP1 identified its pleiotropic roles in stress tolerance. Hypoxia tolerance in the shoots and Al, H+, and low P tolerance is positively regulated by STOP1; in contrast, drought tolerance is negatively regulated by STOP1 via modulation of K+-uptake. It indicates that Al tolerance is regulated both specifically and together with other stress tolerances. In this Research Topic, we would like to understand such complex systems at molecular levels, including identification of molecules involved in Al-signaling such as sensor and regulatory proteins and TFs.
This Research Topic will focus on understanding the molecular mechanisms underlying the signaling cascades involved in Al resistance responses in model plant species as well as crop species. As described, these processes are regulated by a complex network, including crosstalk with other signaling pathways and early and late responses. Identification of such regulatory processes by genetics (including GWAS and chemical genetics), multi-omics, and bioinformatics-based approaches are welcome. Molecular physiological studies focusing on \understanding crosstalk and pleiotropic effects by Al-signaling are also welcome.
• Genetic studies identifying Al signal
• Comparative genomics and molecular physiology of Al tolerance (e.g. studies of STOP1-system in crops)
• Pleiotropy of Al-inducible Al tolerance.
• Novel Al inducible Al resistant mechanisms
Please note descriptive studies that report responses of growth, yield, or quality to Al stress will not be considered if they do not progress physiological understanding of these responses.
