PHYSIOLOGY OF RUST RESISTANCE 89 



VOX BROEMBSEX: I noticed that in your work with Khapli and resistant 

 varieties, you observed a decrease in proteins and RXA, two days after 

 infection. This doesn't seem to go along with the idea of reduction of 

 protein synthesis constituting a disease resistance mechanism. 



SHAW: In Khapli, what we actually found was the same drop in 

 histones, a less marked increase in RXA, and a less marked increase in 

 fast green protein; but these increases were much more transient than in 

 the susceptible variety. I passed over that very fast, I know. The most 

 striking difference, really, between the Khapli situation and the Little 

 Club one is that in Khapli you do get a decrease in DXA, which you will 

 not see in Little Club until the infection is very old. 



DAY: How many of the changes that you describe as occurring follow- 

 ing infection are common to the kind of response which occurs when you 

 injure the plant? In ether words, how many of the changes are specifi- 

 cally induced by a pathogen? 



SHAW: That is a very good question. I think that I am on record 

 in print as saying that we don't know whether, in fact, we are dealing 

 with some sort of specific response to the parasite or whether we are 

 dealing with a less specific response to stress. I don't think you get 

 nearly as extensive a response by injury as you do by infecting a sus- 

 ceptible plant with a parasite which will develop on it. The response 

 of Khapli is much more condensed in time. Things happen quicker, and 

 the whole thing falls off much more rapidly, but I don't think that we 

 really have any critical evidence that these are specific responses. 

 Somehow, we have got to try to determine whether they are specific or 

 not . 



FINCHAM: I was prompted by your remarks on host-parasite relations 

 to think a little more about the gene-for-gene hypothesis we heard about 

 this morning. As I understand this hypothesis, it means that for every 

 gene in the host conferring resistance there is a gene in the parasite 

 that would mutate in one step to overcome this resistance. Looking at 

 it from a physiological point of view, do you see any reason why there 

 should be only one gene in the parasite? 



SHAW: Xo. 



FIXCHAM: .And is this implied in the gene-for-gene hypothesis? 



SHAW: I think we better let the gene-for-gene experts answer that. 

 I , as a non-geneticist, don't see why there should only be one, but let 

 me pass that to our moderator. 



PERSOX: I just have to agree with Dr. Shaw. I would think that 

 having got a resistant host population, we would have a situation that 

 would screen out the more successful members of the parasitic population, 

 and that those that have a gene with a large effect that makes the 

 parasite really successful in this situation will have an advantage over 

 other smaller mutations . But, I don't see that the possibility is 

 excluded of accumulating groups of genes in the parasite in response to 

 a mutation in the host population that makes it resistant. So, I think 

 that your question is well-based. There is no reason that I know of for 

 concluding that you must have a gene-for-gene relationship in every case. 



