94 CO. PERSON 



An important question at this juncture is to ask if anything has been 

 learned of disease resistance in agricultural crops that may be carried 

 over to the study of natural populations. We have heard papers today on 

 gene-for-gene relationships, and on horizontal and vertical resistance. 

 It is evident that the use of major genes can give dramatic results. 

 Because introduction of a major resistance gene can evoke equally dramatic 

 single-gene responses from the parasitic population (this is probably how 

 gene-for-gene relationships originate) , there are many plant breeders who 

 now favor the use of horizontal (i.e., multigenic) resistance. But we 

 heard today also that Dr. Zadoks views the two types of resistance, 

 horizontal and vertical, as representing the outer limits of a resistance 

 continuum that ranges between the two extreme types. Van der Plank also 

 mentions in his book that the terms "horizontal" and "vertical" do not 

 readily accommodate resistance that is intermediate (i.e., digenic or 

 trigenic) . The preference of some breeders for multigenic resistance, 

 and the hope that this kind of resistance may confer longer-term benefits 

 to agriculture, may very well have originated from an oversimplified view 

 of the problem. 



We can also ask whether major and minor genes both have a role to 

 play in naturally occurring populations. When we recall that the demission 

 genes for potato resistance to late blight were in fact collected from 

 naturally occurring wild-potato populations of South America, the answer 

 to this question seems to be "yes". As well, certain major genes for 

 resistance to crown rust have been transferred to cultivated oats, through 

 breeding, from wild populations ot Avena sterilis L. Several other examples 

 of major-gene resistance obtained from species in nature are listed by 

 Watkin Williams (1963). 



Evidence for the existence of horizontal resistance in nature is 

 harder to find. This is not surprising, since the genetic basis for this 

 kind of resistance is inherently difficult to demonstrate. The "field- 

 resistance" of potatoes to late blight seems to have arisen "naturally" 

 (i.e., not through artificial breeding) during the decades immediately 

 following the great potato famine in Europe. There is no good reason, it 

 seems to me, for thinking that this kind of resistance does not also 

 exist, as an integral component, in naturally occurring systems of 

 parasitism. 



Accepting the premise that major and minor genes are both present in 

 naturally occurring systems of parasitism, we can next ask the question: 

 how do they work together in such a way as to regulate the disease? 

 Although there is no good answer to this question as yet, some hints as 

 to possible answers are mentioned below. 



According to Pimental (1961) the specific interactions between 

 "feeding" and "eaten" populations (whether these interactions involve 

 predator-prey, herbivore-plant , or host-parasite relationships) are kept 

 under control in nature through operation of specific regulating 

 mechanisms. The rule, in all these relationships, is that the feeding 

 species must feed without endangering survival of the eaten species. 

 (In financial terms this would be a question of living on the interest 

 without withdrawing the capital) . Some of the evidence for regulating 

 mechanisms is of a negative kind: when a species is introduced as an 

 immigrant to a new community, it commonly increases to outbreak levels in 

 a very short time; we infer that it does so because it is newly freed from 

 its normal regulatory restraints. Pimentel has identified at least one 

 such regulatory mechanism, "genetic feedback", by which interacting species 



