Aluminum (Al) toxicity is the primary limiting factor of crop production on acid soils, which affect much of the earth's arable lands. Traditional plant breeding has been successful in improving crop tolerance to Al toxicity. However, further improvements in crop aluminum tolerance will require a deeper understanding of the underlying molecular and physiological mechanisms. Hence, the research described in this thesis focused on the genetic and molecular basis for aluminum tolerance in wheat and maize. In wheat, two approaches were taken to attempt to isolate Al tolerance genes/proteins. A proteomics-based approach using wheat deletion lines around the major Al tolerance locus was unsuccessful in identifying Al tolerance proteins associated with tolerance. An alternate approach focused on the isolation of putative malate transporters of the CLC (chloride channel) channel family, as wheat Al tolerance is based on Al-activated root malate exudation. Eight representatives of this family were cloned from the Al tolerant wheat cultivar Atlas 66; however, genetic analysis revealed that none of these genes were linked to the wheat Al tolerance locus. The CLC genes exhibit widely different tissue and Al responsive gene expression patterns, suggesting different functions for some of these CLCs. Phylogenetic analysis revealed that the cloned TaCLCs represent only a portion of the entire CLC family present in wheat. In maize, a quantitative statistical analysis of aluminum tolerance was conducted on recombinant inbred lines of the intermated B73 x Mo17 (IBM) population. Five quantitative trait loci (QTL) were identified using composite interval mapping as having a significant impact on Al tolerance. These five regions were not orthologous to genomic regions associated with Al tolerance in wheat, rice, sorghum, rye, or barley. In three QTL, Mo17, which has an extremely high Al-activated root citrate release, contributes the superior allele, and these QTL are likely to contribute to that mechanism. In the two QTL in which B73, which has virtually no citrate release, contributes the superior allele tolerance is likely conferred through an alternative mechanism.