Metabolism of Indoleacetic Acid in Rust Diseases. I. Factors Influencing Rates of Decarboxylation

One of the results of the infection of a higher plant by a pathogen may be a change in the rates of nmetabolism of hormones. It is possible that hormone concentrations are of importance in controlling the development of both host and pathogen. Most obviously, abnormal growth of the host may result from changes in hormones caused by the prolonged development of the pathogen in the host tissue. In such instances, the role of hormones essentially is a side effect of no consequence to parasite establishment. However, it is conceivable that the initial establishment of the pathogen may depend upon hormonal changes caused by the entry of the pathogen. In this second case, the changes may be confined to the few cells at the site of infection or may be too transient to cause malformations, even if the plant organ is competent to respond by growing. Some previous work (14, 16, 23, 24, 34) has shown that higher levels of IAA occur in several plant species infected by rust fungi which cause distinct growth disturbances. Usually the data were obtained in late stages of infection when the parasite was in a phase of spore production rather than vegetative growth. Studies (4, 6) of infection by Puccinia carthami on hypocotyls of safflower suggested correlations among mycelial growth and disease-induced respiration, host growth and quantitative increases in auxin levels. The increase in auxin could be detected in the very early stages of disease. It was postulated that primary contact by the fungus in susceptible tissue triggered an increase in hormones which induced host changes conducive to continued growth of the parasite. It was suggested that factors, possibly metabolic, which are controlled by hormones were common to vegetative growth of both host and parasite. Although it was suggested (31) that IAA might modify pathways of metabolism, subsequent work (5) indicated that the low C./C,