Canadian Forest Service Publications

Molecular evidence of distinct introductions of the European race of Gremmeniella abietina into North America. 1998. Hamelin, R.C.; Lecours, N.; Laflamme, G. Phytopathology 88(6): 582-588.

Year: 1998

Available from: Laurentian Forestry Centre

Catalog ID: 16771

Language: English

CFS Availability: PDF (request by e-mail)

Abstract

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, Ф = 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 (Ф = 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 Newfoundland 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.

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