Mechanisms of Fe-deficiency tolerance and signaling were investigated in shoots of Santi (deficiency tolerant) and Parafield (deficiency intolerant) pea genotypes using metabolomic and physiological approaches. From metabolomic studies, Fe deficiency induced significant increases in N-, S- and tricarboxylic acid cycle metabolites in Santi but not in Parafield. Elevated N metabolites reflect an increase in N-recycling processes. Increased glutathione and S-metabolites suggest better protection of pea plants from Fe-deficiency-induced oxidative stress. Furthermore, Fe-deficiency induced increases in citrate and malate in leaves of Santi suggests long-distance transport of Fe is promoted by better xylem unloading. Supporting a role of citrate in the deficiency tolerance mechanism, physiological experiments showed higher Fe and citrate in the xylem of Santi. Reciprocal-grafting experiments confirm that the Fe-deficiency signal driving root Fe reductase and proton extrusion activity is generated in the shoot. Finally, our studies show that auxin can induce increased Fe-reductase activity and proton extrusion in roots. This article identifies several mechanisms in shoots associated with the differential Fe-deficiency tolerance of genotypes within a species, and provides essential background for future efforts to improve the Fe content and deficiency tolerance in peas.