626 NORMAN E. BORLAUG 



organism that adequately cover the spectrum of pathogenicity of the 

 pathogen throughout the region for which the varieties or cultivars are 

 being bred, and that can penetrate through any specific resistance that 

 may be present. Beware of using wild inoculum from only one local area 

 close to your research center. It may not represent the entire spectrum 

 of the pathogenicity of the pathogen. Have no fears of bringing in wild 

 inoculum for your screen tests from remote areas of your region. If 

 your breeding stocks fall prey to such inoculum it simply means that the 

 genetic base for resistance in your breeding program is too narrow to 

 provide effective protection for a long cutting cycle species such as 

 P. monticola, P. strobus (60 to 80 years) or even for short cutting cycle 

 species such as P. taeda or P. elliottii (25-40 years) . One must remem- 

 ber it took C. ribicola only about 40 years to spread over most of the 

 range of P. monticola even with the Ribes eradication programs trying to 

 hold the spread. Moreover, it is absolutely necessary to obtain the 

 inoculum from a broad spectrum of species and varieties of the alternate 

 hosts (i.e., Ribes spp. or Quercus spp.) to minimize the danger of using 

 too narrow a spectrum of pathogenicity of the rust. 



Rust tests designed to determine the general resistance of progeny 

 must take into consideration: (1) The dosage of inoculum used, (2) the 

 amount of infection produced, (3) the amount of inoculum produced, and 

 (4) the rate of disease spread in host tissue. The inoculation test 

 should measure the biotic balance between the host and pathogen. 



Valvilov 5 (1935) long ago pointed out that the greatest diversity 

 and widest spectrum of genes for pathogenicity of an obligate parasite, 

 such as C. ribicola, as well as genes for resistance in the host, are 

 found in the center of origin of the pathogen, which in this species is 

 most certainly eastern Asia. C. ribicola is also almost probably more 

 variable in its secondary zone of differentiation in Europe than it is 

 in North America. It is possible that only a part of the spectrum of 

 pathogenicity was introduced into North America from Europe. Nor is 

 there any assurance that the culture of C. ribicola introduced into 

 western U.S.A. and now decimating P. monticola is the same as that 

 introduced into eastern U.S.A. on P. strobus. Perhaps rust culture 

 differences in part account for the apparent lower level of effective 

 protection provided by the intraspecific rust-resistance breeding programs 

 on P. strobus as contrasted with that in P. monticola. The short period 

 of time that C. ribicola has been present in North America - 60 to 75 

 years - probably has been too short a period to contribute much to its 

 diversification since introduction. 



All of the aforementioned considerations have important bearings on 

 the choice of sources of parental resistance and on the evaluation of 

 the effectiveness of resistance in current breeding programs . A forest 

 tree breeder could proceed with great confidence if he knew that his 

 parental stocks were resistant to C. ribicola in 5 or 6 areas in eastern 

 Asia where the pathogen is indigenous and endemic, in several locations 

 in the secondary zone of differentiation in Europe, as well as in the 

 region where he is conducting his breeding program. 



Vavilov's hypothesis probably was largely formulated to apply to 

 resistance provided by genes causing hypersensitivity in the host 

 (specific resistance) . It may 3 however 3 also apply at least in part to 

 polygenic general resistance. 



