Originally posted by orangepippin
View Post
Cox has minor resistance gene "A" from its mother and "B" from ist father.
Dr.Oldenburg has minor resistance gene "C" from its mother and "D" from its father.
Think of them as antifungal chemicals which flow in the sap.
Over many years, the fungi have evolved to defeat the AB combination in Cox, or the CD combination in Dr.Oldenburg.
But their offspring will be AC, AD, BC or BD; they are combinations of the two.
Let's call Alkmene AC (A from Cox, C from Dr.Oldenburg)
The AB-specific diseases of Cox are defeated by the presence of C in the offspring from the other parent.
Similarly, the CD-specific diseases of Dr.Oldenburg are defeated by the A inherited from Cox.
However, since the ofspring still share one gene in common with their parents, the fungi are already halfway there to breaking through the resistance. This is a random chance event, modified by some varieties being lucky enough to carry a few additional resistance genes.
It is easier for Cox's AB-specific diseases to get past the single defeating gene of "C" in an "AC" offspring, than to get past the genes "E, F & G" in an old triploid (let's say Boskoop).
To defeat Alkmene, only one mutation is required from the existing Cox disease strains. But to defeat Boskoop (an unrelated variety to Cox) would require three fungal mutations all at once.
So Boskoop's resistance would turn out to be more durable in an orchard of Cox and Cox offspring.
This, of course, would be slightly modified by some offspring being lucky and recieving a few more resistance genes than others (there will, almost certainly, be more than a couple of minor resistance genes in Cox, even if they've been defeated, so my example above is greatly simplified); therefore a bit of variation in the susceptibility of the offspring of Cox.
Comment