Abstract
The production of pectolytic enzymes in vivo and in vitro by S. fructicola and by Rhizopus arrhizus Fischer in vivo is established. Evidence is presented which suggests that the products of fungal pectolysis may constitute a carbon source for the growth in vivo of S. fructicola, and this is discussed in relation to the carbohydrate requirement of the pathogen. The following relations which demonstrate that the pectolytic enzymes of the pathogen play an important part in determining the relative susceptibility to infection of green and ripe fruit have been established: (1) the more mature the fruit, the lower is the spore load required to produce a rot; (2) enzyme production is proportional to spore load; (3) the rapidity of tissue maceration is proportional to spore load; (4) the rapidity of tissue maceration is inversely proportional to the firmness of the tissue. The softening of the fruit tissue during maturation may be correlated with a decrease in the proportion of the middle lamella pectin as ripening progresses. Thus, the unfavorable environment oi the green fruit for the development of the pathogen is partly accounted for by the mechanical resistance of the middle lamella to hyphal spread. The invasion of both green and ripe peach fruit tissue results in comparable losses in the insoluble pectin fraction, but in the former case there is an accumulation and in the latter a depletion in the level of soluble pectin as compared with that in healthy tissue. These results are used to distinguish between the solubilization and the breakdown of the parent pectic materials by the pathogen. Also, they indicate the presence of substances in the green tissue inhibitory towards the pectolytic enzymes. R. arrhizus, which is a soft-rot pathogen, induces greater losses in the pectic materials of ripe peach fruit than does S. fructicola, a firm-rot pathogen. It is suggested that this is due to the greater mycelial density of the former in the tissues.