Abstract. In this study, the role of root organic acid synthesis and exudation in the mechanism of aluminum tolerance was examined in Al-tolerant (South American 3) and Al-sensitive (Tuxpefio and South American 5) maize genotypes. In a growth solution containing 6 ~tM A13+, Tuxpefio and South American 5 were found to be twoand threefold more sensitive to A1 than South American 3, Root organic acid content and organic acid exudation from the entire root system into the bulk solution were investigated via high-performance liquid chromatographic analysis while exudates collected separately from the root apex or a mature root region (using a dividedroot-chamber technique) were analyzed with a more-sensitive ion chromatography system. In both the Al-tolerant and Al-sensitive lines, A1 treatment significantly increased the total root content of organic acids, which was likely the result of A1 stress and not the cause of the observed differential A1 tolerance. In the absence of A1, small amounts of citrate were exuded into the solution bathing the roots. Aluminum exposure triggered a stimulation of citrate release in the Al-tolerant but not in the Al-sensitive genotypes; this response was localized to the root apex of the Al-tolerant genotype. Additionally, AI exposure triggered the release of phosphate from the root apex of the Al-tolerant genotype. The same solution A13+ activity that elicited the maximum difference in AI sensitivity between Al-tolerant and Al-sensitive genotypes also triggered maximal citrate release from the root apex of the Al-tolerant line. The significance of citrate as a potential detoxifier for aluminum is discussed. It is concluded that organic acid release by the root apex could be an important aspect of A1 tolerance in maize.

Although it is well known that aluminum (AI) resistance in wheat (Trificum aestivum) is multigenic, physiological evidence for multiple mechanisms of AI resistance has not yet been documented. l h e role of root apical phosphate and malate exudation in AI resistance was investigated i n two wheat cultivars (AI-resistant Atlas and AI-sensitive Scout) and two near-isogenic lines (AI-resistant E13 and AI-sensitive ES3). I n Atlas AI resistance is multigenic, whereas in E13 resistance is conditioned by the single Alfl locus. Based on rootgrowth experiments, Atlas was found to be 3-fold more resistant in 20 PM AI than ET3. Root-exudation experiments were conducted under sterile conditions; a large malate efflux localized to the root apex was observed only in Atlas and in ET3 and only i n the presence of AI (5 and 20 p~) .Furthermore, the more AI-resistant Atlas exhibited a constitutive phosphate release localized to the root apex. As predicted from the formation constants for the AI-malate and AI-phosphate complexes, the addition of either ligand to the root bathing solution alleviated AI inhibition of root growth in AI-sensitive Scout. These results provide physiological evidence that AI resistance in Atlas is conditioned by at least two genes. I n addition to the alf locus that controls AI-induced malate release from the root apex, other genetic loci appear to control constitutive phosphate release from the apex. We suggest that both exudation processes act in concert to enhance AI exclusion and AI resistance i n Atlas.A1 toxicity is one of the major factors that limits the productivity of crop plants in acid soils. A number of crop species and cultivars exhibit significant genetically based variability in their response to the toxic levels of soil A1 (Kochian, 1995). This variability has served as the basis for a considerable amount of recent research on the underlying mechanisms that result in crop A1 resistance. We are beginning to understand the cellular processes that confer A1 resistance in plants. Most of the recent work has focused on A1 exclusion from the root apex as a primary mechanism of A1 resistance (Kochian, 1995).Root exudation of organic acids that can chelate A13+ in the rhzosphere and, thus, detoxify A1 was first reported in an

No abstract