Boron (B) alleviates aluminum (Al) toxicity in higher plants; however, the underlying mechanisms behind this phenomenon remain unknown. Here, we used bromocresol green pH indicator, noninvasive microtest, and microelectrode ion flux estimation techniques to demonstrate that B promotes root surface pH gradients in pea (Pisum sativum) roots, leading to alkalization in the root transition zone and acidification in the elongation zone, while Al inhibits these pH gradients. B significantly decreased Al accumulation in the transition zone (∼1.0–2.5 mm from the apex) of lateral roots, thereby alleviating Al-induced inhibition of root elongation. Net indole acetic acid (IAA) efflux detected by an IAA-sensitive platinum microelectrode showed that polar auxin transport, which peaked in the root transition zone, was inhibited by Al toxicity, while it was partially recovered by B. Electrophysiological experiments using the Arabidopsis (Arabidopsis thaliana) auxin transporter mutants (auxin resistant1-7; pin-formed2 [pin2]) and the specific polar auxin transporter inhibitor1-naphthylphthalamic acid showed that PIN2-based polar auxin transport is involved in root surface alkalization in the transition zone. Our results suggest that B promotes polar auxin transport driven by the auxin efflux transporter PIN2 and leads to the downstream regulation of the plasma membrane-H⁺-ATPase, resulting in elevated root surface pH, which is essential to decrease Al accumulation in this Al-targeted apical root zone. These findings provide a mechanistic explanation for the role of exogenous B in alleviation of Al accumulation and toxicity in plants.

Summary: P‐type H⁺ ATPases mediate active H⁺ efflux from plant cells. They generate a proton motive force across the plasma membrane, providing the free energy to drive the transport of other solutes, partly by coupling to H⁺ influx. Wegner & Shabala (2020) recently suggested that passive H⁺ influx can exceed pump‐driven efflux due to ‘active buffering’, that is, cytosolic H⁺ scavenging and apoplastic H⁺ generation by metabolism (‘biochemical pH clamp’). Charge balance is provided by K⁺ efflux or anion influx. Here, this hypothesis is extended to net H⁺ efflux: even though H⁺ pumping is faster than backflow via symporters and antiporters, a progressive increase in the transmembrane pH gradient is avoided. Cytosolic H⁺ release is associated with bicarbonate formation from CO₂. Bicarbonate serves as substrate for the PEPCase, catalyzing the reaction from phosphoenolpyruvate to oxaloacetate, which is subsequently reduced to malate. Organic anions such as malate and citrate are released across the plasma membrane and are (partly) protonated in the apoplast, thus limiting pump‐induced acidification. Moreover, a ‘biophysical pH clamp’ is introduced, that is, adjustment of apoplastic/cytosolic pH involving net H⁺ fluxes across the plasma membrane, while the gradient between compartments is maintained. The clamps are not mutually exclusive but are likely to coexist.

Aluminum (Al) toxicity is the primary factor limiting crop growth in acidic soils. Boron (B) alleviates Al toxicity in plants, which is mainly considered to be due to the formation of Rhamnogalacturonan II-B (RGII-B) complexes, which helps to stabilize the cytoskeleton. It is unclear yet whether this is due to the increasing of net negative charges and/or further mechanisms. Kinetics of Al accumulation and adsorption were investigated using entire cells, cell wall and pectin of root border cells (RBCs) of pea (Pisum sativum), to reveal the mechanism of B in interacting with alkali-soluble and chelator-soluble pectin for an increased Al tolerance in RBCs. The results show that B could rescue RBCs from Al-induced cell death by accumulating more Al in the cell wall, predominately in alkali-soluble pectin. Boron also promotes Al3+ adsorption and inhibits Al3+ desorption from alkali-soluble pectin. Thus, more Al3+ is immobilized within the alkali-soluble pectin fraction and less in the chelator-soluble pectin, rendering Al3+ less mobile. Boron induces an increase of RG-II (KDO,2-keto-3-deoxyoctonic acid) content for forming more borate-RGII complexes, and the decrease of pectin methyl-esterification (DM), thus creates more negative charges to immobilize Al3+ in cell wall pectin. The study provides evidence that abundant B supply enhances the immobilization of Al in alkali-soluble pectin, thus most likely reducing the entry of Al3+ into the symplast from the surroundings.

Impacts of biochar application mode on nitrogen (N) leaching, ammonia (NH₃) volatilization, rice grain yield and N use efficiency (NUE) are not well understood. Therefore, a field experiment was conducted to evaluate those impacts in a rice paddy soil received 225 kg N ha⁻¹ from either urea or N-rich wastewater. One treatment received 10 t ha⁻¹ biochar with the basal fertilization, and the other received same total amount of biochar but split applied with the three split N applications with same ratio as N fertilizer split ratio (40%, 30% and 30%). Results showed that N leaching loads were 4.20–6.22 kg ha⁻¹. Biochar one-time application reduced N leaching by 23.1%, and biochar split application further reduced N leaching by 32.4%. Total NH₃ volatilization loss was 15.5–24.5 kg ha⁻¹. Biochar one-time application did not influence the NH₃ volatilization, but biochar split application stimulated the cumulative NH₃ volatilization by 57.7%. Both biochar treatments had no influence on NUE and rice grain yield. In conclusion, biochar application mode indeed influences the N leaching and NH₃ volatilization in rice paddy soils, and biochar one-time application should be recommended for reducing N leaching without increasing NH₃ volatilization.

The initial response of plants to aluminum (Al) is the inhibition of root elongation, while the transition zone is the most Al sensitive zone in the root apex, which may sense the presence of Al and regulate the responses of root to Al toxicity. In the present study, the effect of Al treatment (30 μM, 24 h) on root growth, Al accumulation, and properties of cell wall of two pea (Pisum sativum L.) cultivars, cv Onward (Al-resistant) and cv Sima (Al-sensitive), were studied to disclose whether the response of root transition zone to Al toxicity determines Al resistance in pea cultivars. The lower relative root elongation (RRE) and higher Al content were founded in cv Sima compared with cv Onward, which were related to Al-induced the increase of pectin in root segments of both cultivars. The increase of pectin is more prominent in Al-sensitive cultivar than in Al-resistant cultivar. Aluminum toxicity also induced the increase of pectin methylesterases (PME), which is 2.2 times in root transition zone in Al-sensitive cv Sima to that of Al resistant cv Onward, thus led to higher demethylesterified pectin content in root transition zone of Al-sensitive cv Sima. The higher demethylesterified pectin content in root transition zone resulted in more Al accumulation in the cell wall and cytosol in Al-sensitive cv Sima. Our results provide evidence that the increase of pectin content and PME activity under Al toxicity cooperates to determine Al sensitivity in root transition zone that confers Al resistance in cultivars of pea (Pisum sativum).

Soil acidity (and associated Al toxicity) is a major factor limiting crop production worldwide and threatening global food security. Electrostatic layer-by-layer (LBL) self-assembly provides a convenient and versatile method to form an extracellular silica nanocoat, which possess the ability to protect cell from the damage of physical stress or toxic substances. In this work, we have tested a hypothesis that extracellular silica nanocoat formed by LBL self-assembly will protect root border cells (RBCs) and enhance their resistance to Al toxicity. Scanning electron microscopy (SEM) and X-ray photoelectron spectroscopy (XPS) were used to compare the properties of RBCs surface coated with nanoshells with those that were exposed to Al without coating. The accumulation of Al, reactive oxygen species (ROS) levels, and the activity of mitochondria were detected by a laser-scanning confocal microscopy. We found that a crystal-like layer of silica nanoparticles on the surface of RBCs functions as an extracellular Al-proof coat by immobilizing Al in the apoplast and preventing its accumulation in the cytosol. The silica nanoshells on the RBCs had a positive impact on maintaining the integrity of the plasma and mitochondrial membranes, preventing ROS burst and ensuring higher mitochondria activity and cell viability under Al toxicity. The study provides evidence that silica nanoshells confers RBCs Al resistance by restraining of Al in the silica-coat, suggesting that this method can be used an efficient tool to prevent multibillion-dollar losses caused by Al toxicity to agricultural crop production.