PHYSIOLOGY OF RUST RESISTANCE 91 



ZUFA: Evidently, it doesn't do any damage to the host. 



SHAW: I don't think so. It's quite easy for me to conceive of the 

 two organisms living side by side indefinitely. 



VON BROFMBSEN: You emphasized that you thought there was a need for 

 some good biochemical work on protein synthesis after inoculation. What, 

 in your judgment, would be early, particularly in resistance reactions 

 such as in Khapli where things happen fast? 



SHAW: I don't think the Khapli system is a very good system to work 

 with, but I am interested in what happens in the first 72 hours after 

 inoculation. I am interested in everything that happens during that 

 period. I picked 72 hours because of the results of one specific case 

 that I am thinking about now, and this is with the SR-6 gene. You know 

 there was some work done by Frank Forsythe of Winnipeg a number of years 

 ago which I don't think has been cited enough or thougnt about enough. 

 He went back to the idea of investigating the effect of light and 

 temperature regimes on rust development, and the key point was that he 

 found that whatever race of rust he was using on the variety that 

 carried the SR-6 gene, which is temperature sensitive, he could reverse 

 the situation from resistant to susceptible or susceptible to resistant 

 by changing the temperature in the right direction up to approximately 

 72 hours after inoculation. Beyond that point, let's say it was some- 

 where between 72 and 90 hours, changing the temperature had no effect. 

 So he had reached a point of no return and the thing was set. I think 

 that this is a very important point which has not received enough 

 attention. So early, in my terminology, means 24 to 48 hours. 



VON BROEMBSEN: Did you show any data on protein synthesis for 

 48 hours? 



SHAW: I think the earliest figures showed increased incorporation 

 of leucine into protein as early as 8 hours after infection. 



PERSON: Are there any other questions or comments? 



MCDONALD: I would like to point out one very important aspect of 

 the examples you gave which you didn't exactly state. You have a high 

 degree of genetic control of both host and pathogen. 



SHAW: Right --with the flax system. 



MCDONALD: This is an extremely important point. Further, with 

 respect to our natural system--or a system that hasn't been studied much, 

 this is one of the things that really gives us fits in trying to do 

 physiological work. We just don't have this control yet. 



SHAW: Well, that's true. 



CALLAHAM: For this very reason, do you consider that it is really 

 worth while for us to go into sophisticated physiological studies of the 

 response to infections or the nature of resistance in forest tree systems 

 where essentially we are dealing with the wild host and microorganisms? 



