A collection of 124 isolates of turnip mosaic virus was gathered from around the world, principally from European countries, and characterized by inoculation to four differential lines of Brassica napus (oilseed rape and swede). Three symptom phenotypes were induced—apparent immunity, local infection only, or systemic infection. Twelve distinct patterns, i.e. pathotypes, were observed. Three pathotypes were predominant in the collection; pathotype 1 isolates, which were the most common, did not overcome any of the most extreme sources of resistance in the differential lines. Of the other two, pathotype 3 isolates overcame one of the major sources of resistance and pathotype 4 isolates overcame all sources of resistance. The distribution of pathotypes within Europe was examined. No pathotype was confined to any geographical area, although pathotype 4 isolates were not found in southern Europe or Asia. Most isolates (90) originated from Brassica hosts, while others were from other cruciferae genera (19) or non‐crucifers (5). The species of plant that the isolates originated from was not clearly related to the pathotype of the isolates. Resistance to pathotype 1 isolates is controlled by a dominant allele in one of the differential lines, and resistance sources are being examined in the other lines. Isolates belonging to pathotype 1 appeared to be able to mutate readily to overcome the resistance in one of the rape differential lines, but no isolates appeared to mutate to overcome the other major source of resistance in the differentials. The implications of the results for disease control strategies are discussed.
The viral component of Turnip mosaic virus (TuMV) determining virulence to the Brassica napus TuRB01 dominant resistance allele has been identified. Sequence comparisons of an infectious cDNA clone of the UK 1 isolate of TuMV (avirulent on TuRB01) and a spontaneous mutant capable of infecting plants possessing TuRB01 suggested that a single nucleotide change in the cylindrical inclusion (CI) protein coding region (gene) of the virus was responsible for the altered phenotype. A second spontaneous mutation involved a different change in the CI gene. The construction of chimeric genomes and subsequent inoculations to plant lines segregating for TuRB01 confirmed the involvement of the CI gene in this interaction. Site-directed mutagenesis of the viral coat protein (CP) gene at the ninth nucleotide was carried out to investigate its interaction with TuRB01. The identity of this nucleotide in the CP gene did not affect the outcome of the viral infection. Both mutations identified in the CI gene caused amino acid changes in the C terminal third of the protein, outside any of the conserved sequences reported to be associated with helicase or cell-to-cell transport activities. This is the first example of a potyvirus CI gene acting as a determinant for a genotype-specific resistance interaction.
Dominant resistance genes identified in Brassica napus lines are effective against some, but not all, Turnip mosaic virus (TuMV) isolates. An infectious clone of an isolate (UK 1) was used as the basis of chimeric virus constructions using resistance-breaking mutants and other isolates to identify the virulence determinants for three dominant resistance genes. For the resistance gene TuRB01, the presence of either of two mutations affecting the cylindrical inclusion (CI) protein converted the avirulent UK 1 to a virulent isolate. Acquisition of such mutations had a slight cost to viral fitness in plants lacking the resistance gene. A similar strategy is being used to identify the virulence determinants for two more resistance genes present in another B. napus line.
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