Understanding the delayed expression of Al-resistance in signal grass (Urochloa decumbens).

BACKGROUND AND AIMS: Signal grass (Urochloa decumbens) is a widely used pasture grass in tropical and subtropical areas due to its high Al-resistance. However, the underlying mechanisms conferring this resistance are not clearly understood. METHODS: Al concentrations of bulk root tissues and intracellular compartment were examined, including impact of a metabolic inhibitor carbonyl cyanide m-chlorophenyl hydrazone (CCCP). Next, we examined changes in the properties of signal grass root tissues following exposure to toxic levels of Al, including the cell wall cation exchange capacity (CEC), degree of methylation, and concentrations of cell wall fractions. KEY RESULTS: Although signal grass was highly resistant to Al, there was a delay at 24-48 h before the expression of this resistance. We found that this delay in the expression of Al-resistance was not related to the total Al concentration in the bulk apical root tissues, nor was it related to changes in the Al bound to the cell wall. We also examined changes in other properties of the cell wall, including the CEC, degree of methylation, and changes in the concentration of pectin, hemicellulose, and cellulose. We noted that concentrations of intracellular Al decreased ca. 50 % at the same time that root elongation rate improved after 24-48 h. Using CCCP as a metabolic inhibitor, we found that the intracellular Al concentration increased ca. 14-fold and that the CCCP prevented the subsequent decrease in intracellular Al. CONCLUSIONS: Our results indicate that the delayed expression of Al-resistance was not associated with Al concentration in the bulk apical root tissues or bound to the cell wall, nor was it associated with changes in other properties of the cell wall. Rather, signal grass has an energy-dependent Al exclusion mechanism, and this mechanism requires 24-48 h to exclude Al from the intracellular compartment.