GENETIC INTERACTIONS OF WHITE PINES AND BLISTER RUST IN WESTERN NORTH AMERICA
BB KINLOCH Jr
USDA Forest Service, Institute of Forest Genetics, Berkeley, CA, USA
Background and objectives
Results and conclusions
Estimates of population parameters of Cronartium ribicola in western North America indicate that overall variability is low: only 8% of marker loci were polymorphic, with expected heterozygosities (He) of 2.5%. Yet, population differentiation was high (Gst=0.21), in spite of high outcrossing. This apparent paradox may be explained by a combination of genetic drift due to founder effects of single or few aeciospores establishing new infection centres after long-distance dispersal from source populations, and low gene flow in spermatia, the gametic spore stage, which has limited mobility . The epidemiological unity that characterized the spread of blister rust across Europe and then to both coasts of North America implies a corresponding genetic unity. No private alleles were found in any of the western or eastern North American populations sampled, and all may share the same gene pool as the European populations from which they derive. Variation in virulence appears limited; none was found to resistant Ribes cultivars after extensive trials in Europe and North America. On pines, only two races are confirmed. These specifically neutralize major gene resistance (MGR) in sugar pine and western white pine. Virulence to MGR in sugar pine is evidently conditioned by a single plasmagene. Both races appear to have limited distributions. Other virulent races may exist in North American populations, but a greater threat may lie in new introductions from Asia, the ancestral gene centre of the pathogen.
The specificity that exists in this non-co-evolved pathosystem among major genes is intriguing. For example, MGR in sugar pine is not affected by the presumed gene for virulence to MGR in western white pine, and vice versa. This simple complementary structure may represent a nascent gene-for-gene system.