Pectic acid had the most adverse effect on growth of cultured western white pine 

 cells. Although no changes were noted in concentrations of 0.025 percent or less, 29 

 percent of the explants in the 0.05 percent treatment showed no proliferation and 40 

 percent of those showing cell multiplication had browned by the end of the test. 

 Only 14 percent of the explants submerged under a 0.1 percent concentration of pectic 

 acid had produced a visible increase in numbers of cells; however, at the end of the 

 test all explants were brown. The 0.5 percent treatment, in addition to causing 

 browning, inhibited growth of all explants. 



Within the first to second week of exposure the blister rust fungus isolates 

 began to respond to the pectic compounds. Both isolates exhibited suppressed but 

 different growth rates, as shown in fig. 1. Sodium polypectate suppressed growth the 

 least. Polygalacturonic acid, pectic acid, and citrus pectin were the most effective 

 in retarding growth of both isolates with polygalacturonic acid being the most detri- 

 mental to the slow growing isloate. 



Figure 1. --Growth responses of two 

 Cronartium ribicola isolates to 

 pectin compounds. 



, Sodium polyectate 

 ' No treatment 



(fast- growing, isolate) 



No treatment 

 (slow- growing, isolate) 



/" 



— — Sodium polypectate 



y ^^„,„i»—i Citrus pectin 



^^^^^^ Polygalacturonic acid 

 / ^^^^ Pectic acid 



/ ^ Pectic acid 



J II tj _ 



' Polygalacturonic acid 



1 2 3 4 5 6 7 

 TIME (WKS) 



DISCUSSION 



The frequency of cell penetration by haustoria, wherever western white pine bark 

 cells and the blister rust fungus make contact, implies that in a susceptible host- 

 pathogen interaction products of enzymatic actions on native pectin are involved. In 

 other studies, histochemical reactions and localized changes in electron density in 

 the region of penetration suggest that carefully controlled enzymatic interactions 

 between host and pathogen do occur. The extent of enzymatic alterations of cell wall 

 pectins and other products generated by the invading pathogen are unknown. 



3 



