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

The role of AI interactions with root-cell plasma memhrane (PM) Ca2+ channels in AI toxicity and resistance was studied. l h e experimental approach involved the imposition of a transmembrane electrical potential (via K+ diffusion) in right-side-out PM vesicles de- Proc Natl Acad Sci USA 91: 3473-3477). W e found that AI3+ effectively blocked this P M Cazf channel; however, AI3+ blocked this Ca2+ channel equally well in both the AI-sensitive and -resistant cultivars. I t was found that the differential genotypic sensitivity of this Ca2+ transport system to AI in intact roots versus isolated PM vesicles was due to AI-induced malate exudation localized to the root apex in AI-resistant Atlas but not in AI-sensitive Scout. Because malate can effectively chelate AI3+ in the rhizosphere and exclude it from the root apex, the differential sensitivity of Ca2+ influx to AI in intact roots of AI-resistant versus AI-sensitive wheat cultivars is probahly dueto the maintenance of lower AI3+ activities in the root apical rhizosphere of the resistant cultivar.A1 toxicity is the primary environmental stress limiting crop productivity on acid soils. One of the proposed mechanisms of A1 toxicity involves A1 interaction with ion transport systems functioning at the root-cell PM (Taylor, 1988;Kochian, 1995). The role of A1/Ca2+ transport interactions in the mechanisms of A1 toxicity has recently received considerable attention, because Ca2+ plays a central role in the regulation of many plant cellular processes, including mitosis and cytokinesis, gravitropism, polar growth, and cytoplasmic streaming (Williamson and Ashley, 1982;Hepler and Wayne, 1985). A1 inhibition of Ca2+ influx into plant cells is rapid and reversible, and the A1 blockage of Caz+ influx precedes visible symptoms of A1 toxicity (Huang et al