Although the basic mechanism of action of plant hormones is not known, there is some evidence that indole-acetic acid (IAA) exerts an effect on pathways as well as rates of respiratory metabolism (7, 9,10,15). The influence of plant hormones on metabolism may be critically important to understanding obligate parasitism. There is evidence that IAA increases as a consequence of infection by rust fungi (3, 14). Applications of growth regulators alter the degree of susceptibility of wheat to stem rust (16, 17). Daly and Sayre suggested that hormonal imbalance in the early stages of infection could act as a stimulus to increase host metabolism moderately (5). Subsequent increases in respiration during sporulation of rust fungi were postulated to arise from parasite metabolism. The large increases observed at sporulation are characterized by low C6/C1 ratios indicating different pathways of sugar catabolism (2, 5). The demonstration by Humphreys and Duggar (9, 10) that hormonal treatments induce low C,6/C1 ratios in roots raises the question as to whether the Iow C61C1 ratio in disease might occur in host cells by hormonal induction. Although preliminary data in this laboratory indicated that hormones did not influence C6/C1 ratios with bean tissue, Shaw et al. (15) reported that brief exposure (1? hr) of normal wheat leaf sections to 5.0, 8.3, and 16.6 ppm of IAA resulted in C6/C1 ratios approximating those obtained by rust infections. They noted, however, that hormonal treatments induced low ratios by reducing C6 recovery while, in their experience, rust-affected leaves had enhanced C1 recovery. For this reason they did not definitely implicate IAA as a triggering agent for the metabolic alteration of diseased tissue. It has been shown recently (2) that the decline in C6/C1 ratios in disease tissue can be effected either by low C6 or by high C1 recovery when compared to control tissue. At the time lower C6/C1 ratios first were apparent, the effect was due to lower percentage of recoveries from the sixth carbon of gluoose. If infections were heavy, greater recovery from the Cl carbon occurred in the later stages of disease development. Further, the data of Humphrey and Duggar indicate that hormonal treatments do not produce a consistent effect on C1 or C6 recovery. Consequently, the existing data do not eliminate hormonal imbalance as a causal factor in the establishment of pathological deviations in metabolism. Although a decline in C1/C, ratios with infection occurs under a range of environmental conditions and tissue types (2), the influence of hormones on growth and metabolism often is dependent on specific environmental conditioning of responsive tissues. Our data were obtained in an effort to establish whether or not hormones consistently alter metabolic pathways in healthy and rust affected tissues of several species.