18 P. R. DAY 



FLOOR DISCUSSION 



PERSON: You suggested that the basis for aggressiveness of the rust 

 may be polygenes, numerous genes with small effects. Would you expand on 

 this a tiny bit? 



DAY: The genetic control of fitness or aggressiveness is likely to 

 be much the same as that of stature, vigor, weight and other characters 

 of this kind in higher organisms. They are the culmination of many dif- 

 ferent processes in the organism. The effects of single genes are detec- 

 table but generally you would expect continuous variation among genetically 

 different individuals in a population. 



PERSON: Would you suggest that the counterpart to aggressiveness in 

 the host in terms of resistance is field resistance? 



DAY : Yes . 



PERSON: That's the point I was interested in. 



KINLOCH: I have a question for Dr. Day. Would you expect the 

 potential for new virulent races of white pine blister rust to be com- 

 parable to that in the cereal rusts? Since we are concerned with a haploid 

 stage which is a product of meiosis and has undergone genetic recombina- 

 tion there is less potential for an explosive buildup of uniform genotypes 

 such as you have in a uredospore population of wheat rust. I would like 

 to bring up another point. If resistance depends on several things, then 

 presumably there are several resistance genes in a host. The pathogen has 

 to have virulence genes to combat them. If it has to go through meiosis 

 there is a chance of an appropriate virulent combination arising in many 

 cases. In forestry we are not worried about harvesting the entire crop. 

 We can afford some susceptibility. If we have good genetic resistance in 

 part of the population and let the pathogen take its toll in the other 

 part what does this imply in terms of selection pressure on the pathogen 

 to generate new races virulent on the resistant portion of the crop. I 

 am thinking of van der Plank's hypothesis that the most fit races are 

 usually those with the fewest necessary genes for virulence. These will 

 tend to propagate themselves as long as there are some suscepts in the 

 population and selection pressure is not too extreme against them. 



DAY: In reply to your first question, it seems to me there is no 

 overriding reason for assuming that Cvonavtium is much different from 

 other pathogens in its potential for producing new virulent races. The 

 dikaryotic aecio- and uredospore stages on Bibes store variation and you 

 might imagine on that host there would be little or no direct selection 

 for factors controlling aggressiveness on white pine. You can compare 

 Cronartium with the smuts, where host infection follows meiosis and there 

 is no clonal reproduction of adapted genotypes, or with apple scab, where 

 although clonal reproduction occurs, tree infection begins anew each 

 spring with haploid meiotic products. There seem to be no barriers to the 

 development of virulent forms in these fungi. I would agree that their 

 development and spread has not been as explosive as in the cereal rusts. 

 Now, I don't know how my reply affects your subsequent questions. Perhaps 

 someone else would care to comment. 



PERSON: I believe that the second and third parts of your question 

 will come up more appropriately after we have heard from Dr. Zadoks. 



