SUMMARYMonoterpene and isozyme loci, used as markers to study the genetic structure of Scots pine {Pinus sylvestris L.) native to Scotland, showed that the endemic populations are not genetically impoverished, in spite of severe contraction in range and numbers as a result of both natural and anthropogenic causes. On the contrary, variability in the relict populations is almost the highest of any plant species studied, with average heterozygosities of 0-33 for monoterpenes (five loci) and 0-30 for isozymes (16 loci). The overwhelming proportion of this variability (> 95 "") was within populations, even though significant differences in gene frequencies of many individual loci existed among populations. Multiple-locus comparison of gene frequencies among populations, resolved by canonical variate analysis, showed no coherent geographic pattern of differences from population to population or region to region, with one major exception: certain populations in northwestern Scotland (Wester Ross) were distinct from all others and each other. The pattern of variability of the biochemical markers was consistent with that of metrical and physiological traits reported in the literature. These traits, in turn, show relatively little genetic affinity between eonteniporary Scottish and continetital European populations. The genetic evidence, together with the anomalous distribution of pine pollen in the British Isles during the Holocene, suggests that the Caledonian race of Scots pine originated endemically from more tban one refugium after the last glaciation.

After a full century in North America, the blister rust epidemic has yet to stabilize, continuing to spread into warmer and drier areas previously considered climatically inhospitable. The disease apparently has no environmental limits wherever white pines and Ribes spp. cohabit and will eventually become pandemic. Although much timber value has been lost, more severe long-term damage is disruption caused to ecosystems by altered patterns of natural succession. During the last half of the century just past, development of genetic resistance superceded other direct control measures-mainly Ribes spp. eradication and antibiotics-which proved ineffective and/or unfeasible in large areas of the white pine range, especially in the West. Several mechanisms of complete (major gene) and partial resistance are common to at least several white pine species. Although North American populations of rust have low genetic variability overall, rust genotypes with specific virulence to major resistance genes exist in some local demes at high frequencies. The challenge will be to package and deploy resistance genes in ways that will dampen sudden increases in rust races of wide virulence. New introductions of blister rust from its gene center in Asia remain the gravest threat to genetic improvement programs.

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.