No abstract

The population structure of Cronartium ribicola from eastern and western North America was studied to test the null hypothesis that populations are panmictic across the continent. Random amplified polymorphic DNA markers previously characterized in eastern populations were mostly fixed in western populations, yielding high levels of genetic differentiation between eastern and western populations (phi(st) = 0.55; theta = 0.36; P < 0.001). An unweighted pair-group method, arithmetic mean dendro-gram based on genetic distances separated the four eastern and four western populations into two distinct clusters along geographic lines. Similarly, a principal component analysis using marker frequency yielded one cluster of eastern populations and a second cluster of western populations. The population from New Mexico was clearly within the western cluster in both analyses, confirming the western origin of this recent introduction. This population was completely fixed (H(j) = 0.000; n = 45) at all loci suggesting a severe recent population bottleneck. Genetic distances were low among populations of western North America (0.00 to 0.02) and among eastern populations (0.00 to 0.02), indicating a very similar genetic composition. In contrast, genetic distances between eastern and western populations were large, and all were significantly different from 0 (0.07 to 0.19; P < 0.001). Indirect estimates of migration were high among western populations, including the number of migrants among pairs of populations (Nm > 1) between New Mexico and British Columbia populations, but were smaller than one migrant per generation between eastern and western populations. These results suggest the presence of a barrier to gene flow between C. ribicola populations from eastern and western North America.

The presence of the European (EU) race of Gremmeniella abietina var. abietina, the causal agent of Scleroderris canker of conifers, was first reported in North America in 1975 in the northeastern United States and subsequently in southern Quebec and Newfoundland during the late 1970s, where it quickly became established. We analyzed DNA profiles in samples from a historic collection of G. abietina var. abietina that included some of the first isolates of the EU race reported in the United States to test hypotheses concerning the G. abietina var. abietina epidemic in North America. Genetic diversity was partitioned by an analysis of molecular variance with haplotype frequencies and distances. Genetic differentiation was high between populations in continental North America and Newfoundland (between region differentiation, Phi(ct) = 0.665, P < 0.001). This result was not consistent with the hypothesis of a single introduction of the pathogen into the northeastern United States followed by secondary spread into northeastern Canada. In contrast, small levels of genetic differentiation were observed among continental North American populations (Phi(ct) = 0.047, P = 0.079), suggesting gene flow among these populations. A single haplotype of G. abietina var. abietina dominated the continental populations (80% of the isolates) but was absent from Newfoundland and Europe. Five haplotypes were found in the New-foundland population, all of which were either absent or very rare on the continent. Populations from continental North America clustered together and were distinct from a second cluster composed of European and Newfoundland populations. A phylogenetic analysis of the haplotypes indicated that some of the rare haplotypes may have derived from somatic mutations, whereas others probably occurred as the result of new introductions. The results are consistent with a scenario of distinct primary introductions of this pathogen into Newfoundland and continental eastern North America followed by secondary asexual propagation.

The cellular distribution of laccase Li during degradation of wood chips by Rigidoporus lignosus, a tropical white rot fungus, was investigated by using anti-laccase Li polyclonal antisera in conjunction with immunolabeling techniques. The enzyme was localized in the fungal cytoplasm and was associated with the plasmalemma and the fungal cell wall. An extracellular sheath, often observed around fungal cells, often contained laccase molecules. Diffusion of laccase within apparently unaltered wood was seldom observed. The enzyme penetrated all degraded cell walls, from the secondary wall toward the primary wall, including the middle lamella. Xylem cells showing advanced stages of decay were sometimes devoid of significant labeling. These data suggest that the initial attack on wood was not performed by laccase Li of R. lignosus. Previous alteration of the lignocellulose complex may facilitate the movement of laccase within the wood cell walls. This immunogold study revealed that laccase localization during wood degradation seems limited not in space but in time.