Comparison of the early response to aluminum stress between tolerant and sensitive wheat cultivars: Root growth, aluminum content and efflux of k+

In order to characterize the mechanism of A1 tolerance (Atlas 66) and A1 sensitivity (Scout 66) in two cultivars of wheat (Triticum aestivum L.), the early responses to A1 stress under acidic conditions were investigated. Marked inhibition of root elongation of Scout was observed upon treatment with 10 pM AICI3 for less than 3 h. The inhibition of root elongation of Scout was reversed within 3 days when the treated samples were transferred to a solution without Al. However, treatment for 6 h with AICI3 repressed root elongation almost completely and irreversibly. Root elongation of Atlas was only partially inhibited by the treatment with 10 jim aici3for more than 6 h. Levels of Al in two portions of roots, namely, portions 0–5 mm and 5–10 mm from the tip, were lower in Atlas than those in Scout. In Atlas the levels of Al on a fresh weight basis in both portions were very similar, while the level of Al in the portion 0–5 mm from the tip was almost double than that in the 5–10 mm portion in Scout. A distinct increase in levels of Al in the 0–5 mm portion over that in the 5–10 mm portion of Scout was observed even after 3 h of treatment with AICI3. Both Atlas and Scout were preloaded with K⁺ at pH 5.5 and transferred to distilled water at various pH values to monitor the efflux of K⁺. A reduction in the pH induced increases in the efflux of K⁺ in both cultivars, and the rate of efflux in Scout was twice that in Atlas at pH 4.2. AICI3 at concentrations as low as 5 p. M markedly repressed K⁺efflux at pH 4.2 and this effect was more pronounced in Scout. Ca+ also had a repressive effect on K⁺ efflux, while EGTA increased K⁺ efflux. Vanadate increased K⁺ efflux, a result that suggests the involvement of a H⁺ pump in K⁺ efflux. Ca+ failed to repress the increased efflux of K⁺ caused by vanadate while A1 repressed the K⁺ efflux even in the presence of vanadate. These results suggest that a low extracellular pH may cause an increase in the cytoplasmic concentration of H⁺ that is followed by depolarization of the plasma membrane, which may be modified by the efflux of K⁺ and H⁺. The characteristic difference in terms of K+ efflux between Atlas and Scout at low pH may be caused by differences associated with plasma membrane potentials, as follows. The net influx of H⁺at low pH, which causes depolarization of the plasma membrane, is higher in Scout than in Atlas. The difference in the net influx of H⁺ may be regulated in part by Ca2+, that either repress the influx of H⁺ or the activate of the H⁺ pump. Inhibition of K⁺ efflux by Al, which tends to depolarize the plasma membrane at low pH, may be an important factor in determining sensitivity and/or tolerance to Al.