Temperature-induced susceptibility of soybeans to Phytophthora megasperma f.sp. glycinea: phenylalanine ammonia-lyase and glyceollin in the host; growth and glyceollin I sensitivity of the pathogen

In unwounded soybean hypocotyls, pulse labelled with [¹⁴C]phenylalanine and inoculated with Phytophthora megasperma f.sp. glycinea, rates of [¹⁴C]-incorporation and glyceollin I accumulation were higher in resistant than in susceptible responses throughout the time-course of the experiment. This distinction was masked in hypocotyls that were wounded and inoculated. In such hypocotyls, high rates of [¹⁴C]-incorporation developed that were similar for the first 11 h in resistant and susceptible responses, although much more glyceollin I accumulated in the former. High rates of [¹⁴C]-incorporation also developed in uninoculated wounded hypocotyls but only small amounts of glyceollin I of high specific radioactivity were detected. Estimates of phenylalanine ammonia-lyase activity indicated that the metabolic flux through phenylalanine was limited in wounded controls but potentially very high in resistant responses. Differences in rates of [¹⁴C]-incorporation and in specific radioactivity of accumulated glyceollin I presumably indicate differences in the relative contributions of mobile internal pools and externally applied phenylalanine, in addition to rates of biosynthesis. Rapid decline in [¹⁴C]-glyceollin I was demonstrated in wounded controls in pulse-ch0ase experiments with phenylalanine as chase, but not in inoculated hypocotyls, due to continued [¹⁴C]-incorporation during the chase period. Rapid metabolism was demonstrated in all interactions and in wounds when cinnamic acid was used as the chase, but there was no evidence that differences in glyceollin I accumulation were due to differential rates of metabolism. Additional evidence for metabolic activity was provided by pulse feeding with [¹⁴C]glyceollin I. It is concluded that the stimulus of wounding or infection induces a metabolic pathway in which glyceollin I is not an end product. The accumulation of higher levels of glyceollin I in resistant than in susceptible responses appears to be due to earlier initiation and subsequently higher rates of biosynthesis in the former.