We touched on polyploidy in genetics of course but I don't recall anything that was particularly salient insofar as resistances. In humans xploidy typically res

We touched on polyploidy in genetics of course but I don't recall anything that was particularly salient insofar as resistances. In humans xploidy typically results in either excessive protein expression or compromised (≤50%) protein expression - in many cases this is fatal or seriously damaging in terms of fertility/development. There are exceptions, for instance the mammalian liver has polyploidal cells. But plants are way different in terms of habit, think about evolving to sit in the same place for a hundred years... These for example could have epigenetic crosstalk between their environment (epiphytic nature) and their hosts. E.g. a special chromosome for birch vs oak. Or drought vs monsoon. Given the endpoint of the species is purportedly 350mn years it stands to reason that a highly specialized and nuanced system of regulatory pathways may have emerged. Sequence data and genomics would be revelatory. It wouldn't surprise me if there was specialized information per-host which was regulated by signal produced by the host, I think this would explain redundancy pretty well. Different epigenetic pathways operating on different x¹ chromosomes yielding differential response to discrete small molecules/proteins/hormones produced by host species which prove beneficial in the looong run. This could have a whole cascade of effects or just subtle SNP differences which yield fitness enhancements. Essentially each one being a subroutine for each host case producing local optimums. But I'm just a scrubby undergrad so with a grain of salt. There's probably many other more reasonable explanations, it's biology, biology seeks to find exceptions to every rule by its nature.