A major gene for resistance to white pine blister rust in Western white pine from the Western cascade range.

ABSTRACT A dominant gene for resistance to white pine blister was indicated by Mendelian segregation in full-sib families of western white pine parent trees selected for phenotypic resistance in six heavily infected stands in the Western Cascades of Oregon and Washington. Seedlings were artificially inoculated three times between 1959 and 1964 and observed for development of stem infection. Segregation at this locus (Cr2) occurred in only two of the six parent populations sampled: one a natural stand, Champion Mine (CM), and the other a plantation of unknown seed origin. At CM, reduced penetrance of this gene was expressed by altered Mendelian ratios (mostly less-than-expected resistant phenotypes) in families of specific combinations of certain parents, indicating the presence of modifier genes with effects that ranged from mild to almost complete suppression of Cr2. Between 1968 and 1994, an apparent shift in virulence at CM caused all of the resistant selections to become infected and die. Recent inoculations of many of the same or related families from these parents, made from grafted ramets in a seed orchard, showed that Cr2 conditions a classical hypersensitive reaction (HR) in needle tissues, the primary infection courts. In the latter tests, seedlings were challenged with wild-type and four other sources of inoculum at and near CM that were also suspected of having wider virulence than wild type. No seedlings segregating for HR that were inoculated with wild type subsequently developed stem symptoms, but the other inocula induced both susceptible and HR needle spots on Cr2- genotypes, and many of these seedlings did develop stem infections. This implied that spore genotypes with specific virulence to Cr2 are carried in these inocula.