PHYSIOLOGY AND BIOCHEMISTRY OF RESISTANCE TO PINE RUSTS 46 9 



These data indicate that fusiform rust resistance in shortleaf pine 

 is not a matter of growth substances being limiting for gall development, 

 since infection stimulated auxin and gibberellin production equally in 

 both species. 



The infection-enhanced auxin levels found in these experiments might 

 result either from accelerated auxin production, or from greater auxin 

 stability because of an accumulation of polyphenolic IAAO inhibitors 

 (Hare, 1964). Assuming auxin catabolism to be suppressed, activities of 

 both IAAO (see Lipetz, 1959) and PPO, which spares IAAO from inhibitors, 

 should be attenuated. Instead, in 15 trials, inoculation consistently 

 increased the activity of IAAO and PPO and decreased IAAO inhibitor con- 

 tent in both species for 2 to 5 months following injection. Thus, even 

 though infection increased auxin levels, it also promoted auxin catabolism, 

 assuming that these enzymes regulate auxin breakdown in vivo. Since 

 Galston and Dalberg (1954) showed that IAAO is an inducible enzyme, the 

 enhanced IAAO activity may also be a result of high auxin levels. Short- 

 leaf pines consistently had higher PPO activity than slash--a possible 

 indication that shortleaf has a resistance mechanism based on oxidation 

 of phenols to more toxic quinones . 



PHENOLS 



The participation of phenolics in plant disease resistance is well 

 known. Infection almost invariably leads to accumulation of phenolics 

 and increased respiration due to uncoupling of oxidative phosphorylation 

 by the phenols and enhanced PPO activity (Farkas and Kiraly, 1962; Hare, 

 1966). In the hypersensitive reaction, phenols of host or pathogen origin 

 are oxidized to quinones by PPO. The quinones inactivate enzymes and 

 kill nearby host cells, causing hypersensitive flecking. If the obligate 

 fungus is not killed directly by the quinones, it cannot survive in the 

 necrotic lesions. This mechanism has been well authenticated with cereal 

 rust (Farkas and Ledingham, 1959; Kiraly, 1959; Noveroske, Williams, and 

 Kuc, 1962; Chigrin and Aleshin, 1965). 



Several studies have been made of the relation of phenols to white 

 pine blister rust resistance. The higher tannin content in resistant 

 periderm tissue has already been mentioned, and Of ford (1940) reported 

 more tannins in resistant Ribes leaves. Boyer (1964) and Boyer and 

 Isaac (1964) found that phenols were released from eastern white pine cell 

 vacuoles after rupture of the tonoplasts by the mycelium. The failure 

 of tonoplasts in old cells to rupture until late in the development of 

 the disease may account for the lower resistance of old needles. Among 

 more than 50 phenols examined, Hanover and Hoff (1966) found no qualita- 

 tive differences that could be related to western white pine resistance, 

 but one phenol seemed more abundant in resistant trees. Hoff (1968) 

 found that oxidation of pine extracts with peroxide, as might occur in 

 vivo with PPO, increased their fungitoxicity . 



