528 RAYMOND J. HOFF AND GERAL I. MCDONALD 



data will be re-evaluated. However, it is clear that needle lesion 

 frequency is a resistance factor within the red and yellow spot forming 

 races . 



6. A recessive gene controls the premature shedding of infected 

 needles (McDonald, 1969) . 



7. A recessive gene controls a fungicidal reaction in the vicinity 

 of the short shoot (McDonald, 1969) . 



8. Differential inhibitory compounds in the foliage may partially 

 explain needle resistance. 



9. Slow fungus growth exists in certain resistant plants (McDonald, 

 1969) . 



Resistance believed to be controlled by single dominant genes has 

 been observed in P. lambertiana Dougl . and P. montioola (Barnes, 

 personal communication) and in P. lambertiana (Kinloch, Parks, and Fowler. 

 1970) . 



ACQUISITION AND MAINTENANCE OF LONG-TERM RESISTANCE 



Incorporating rust resistance genes into tree planting stock will 

 require much knowledge, time, and money because of the long generation 

 time (10 to 15 years in western white pine) and the problem of selecting 

 those resistance genes that will assure a high percentage of surviving 

 trees and thus a profitable crop. 



Several methods being tested by breeders of agronomic crops aim at 

 the production of highly resistant and long-lasting varieties. Which of 

 these might be best suited for a long-lived, long-rotation plant like 

 western white pine? Should tree breeders chance factors giving differ- 

 ential resistance, or should such types be dropped, and all efforts 

 concentrated on uniform resistance and/or tolerance'' The scheme chosen 

 might determine the fate of the species as an economical crop. 



CLASSICAL METHODS FOR INCORPORATING RESISTANCE INTO PLANTING STOCK 



Agronomists have devised three general schemes in trying to meet the 

 constant challenges to resistance made by a continually evolving rust 

 fungus . 



Scheme 1 



In scheme 1 we assemble as many different types of differential 

 resistance as possible, combining them in a "synthetic" variety before 

 releasing it for planting stock (Harberd, 1964) . Here, to successfully 

 parasitize this synthetic variety, the pathogen must contain all the 

 required virulence genes at the same time. The chance of their simul- 

 taneous occurrence by mutation and/or recombination is remote. The 

 difficulty with this method, as pointed out by Harberd, is that varieties 

 already present may contain some of the same factors for resistance thus 

 providing a "bridge" across which the pathogen can reinvade at a faster 

 than anticipated rate. Breeders may also inadvertently break up the 

 synthetic variety while selecting for other traits. Both possibilities 

 enable the pathogen to accumulate the needed virulence genes one or a 



