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Breakdown of Host Resistance by Independent Evolutionary Lineages of Beet necrotic yellow vein virus Involves a Parallel C/U Mutation in Its p25 Gene

Breakdown of sugar beet Rz1-mediated resistance against Beet necrotic yellow vein virus (BNYVV) infection was previously found, by reverse genetics, to be caused by a single mutation in its p25 gene. The possibility of alternative breaking mutations, however, has not been discarded. To explore the natural diversity of BNYVV in the field and its effects on overcoming Rz1, wild-type (WT) and resistance-breaking (RB) p25 genes from diverse production regions of North America were characterized. The relative titer of WT p25 was inversely correlated with disease expression in Rz1 plants from Minnesota and California. In Minnesota, the predominant WT p25 encoded the A₆₇C₆₈ amino acid signature whereas, in California, it encoded A₆₇L₆₈. In both locations, these WT signatures were associated with asymptomatic BNYVV infections of Rz1 cultivars. Further analyses of symptomatic resistant plants revealed that, in Minnesota, WT A₆₇C₆₈ was replaced by V₆₇C₆₈ whereas, in California, WT A₆₇L₆₈ was replaced by V₆₇L₆₈. Therefore, V₆₇ was apparently critical in overcoming Rz1 in both pathosystems. The greater genetic distances between isolates from different geographic regions rather than between WT and RB from the same location indicate that the underlying C to U transition originated independently in both BNYVV lineages.