308 K. STERN 



BINGHAM: Dr. Stern, did I misinterpret something you said, that 

 heritability tended to increase as infection became more intense? 



STERN: No, I said that the proportion of non-additive genetic 

 variance in the total genetic variance increased, thus that heritability 

 decreased (see this paper; and Table 4, Bingham et dl. s 1969). 



POPE: I'm a wheat breeder for the University of Idaho, not a 

 forester. I don't use genetic models (except to get a clear picture of 

 the generalized binomial expansion) nor read the literature on herita- 

 bility and genetic gain, but for 20/ years now I have been able to handle 

 the resistance. For about 10 years I have used specific resistance genes 

 that worked just like people say they do and collapsed just like people 

 say they do. In 1960 there was superimposed on our wheat populations 

 rather heavy and uniform, natural spore showers of stripe rust (P. 

 striiformis) that Miss Fuchs talked about (see Fuchs , these proceedings). 

 At that time my wheat populations were mostly efforts to sample the world 

 sources of resistance for bunt {Tilletia spp.) , that were mostly the 

 specific gene type. To my surprise we had also sampled a large number of 

 sources for resistance to stripe rust, in a far more sensible manner than 

 we could have been able to do deliberately. In particular I found the 

 usual specific system (or what I assume was, we didn't bother to find out) 

 of dominant genes that gave good resistance located in varieties where 

 people said they were. In addition to this--in what I assume is our 

 uncomplicated race situation--in most of the varieties other people said 

 were susceptible to stripe rust I found from 1 to 3 or more genes for 

 resistance. In the old, hard red spring wheat Marquis, that is mentioned 

 in the literature as being a useful susceptible check, I found 3 resis- 

 tance genes. In almost every cross I had made for other purposes I found 

 additive interaction for resistance to stripe rust. This follows one of 

 Dr. Stern's models. However, the most striking thing was that some of 

 the spectacular interactions came from wheats that were phenotypically 

 susceptible. It's unfortunate that we must use these descriptive words, 

 because there are only 2 or 3 of them--resistant , susceptible, and 

 immune, with modifying words--while there is a much broader genetic 

 behavioral range. Also, it's a sliding scale. A disease at a given level 

 gives effects you can see with your eyes at one place on the scale. If 

 the disease severity is worse, you slide up the scale and don't see the 

 bottom part of the scale at all. It's my opinion that this is an example 

 of non-specific, multigenic resistance systems, one that is quite wide- 

 spread and more common than the much better known gene-for-gene relation- 

 ships. Philosophically I suspect there is a spectrum of different resis- 

 tance systems that are complimentary to one another. Most wheats with 

 "susceptible" phenotypes turned out to carry genes that contributed to 

 increased resistance in the best propgeny of appropriate crosses. 1 Wheats 

 with "zero" genes for resistance to stripe rust (such as the white spring 

 wheat Lemhi) are rare. As pointed out some of these genes are spectacularly 

 additive with other genes--possibly functioning in a series of chemical 

 reactions where each gene controls one reaction. Without rust there's 

 nothing very useful for the gene, or the complex of genes, to do. I think 

 that in a crude way this situation is comparable to the white pine blister t 

 rust, except that there are probably more resistance-genes scattered in 

 wheats. I found these genes in wheats coming from continents such as 



1 Editors note: See Pope, W. K. 1968. Interaction of minor genes 

 for resistance to stripe rust in wheat, p. 251-257. In Proa. 3rd Int. 

 Wheat Genet. Symp. 3 Canberra. 479 p. 



