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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

February 2010 , Volume 100 , Number  2
Pages  127 - 133

Rodolfo Acosta-Leal, Becky K. Bryan, Jessica T. Smith, and Charles M. Rush

Texas AgriLife Research, Texas A&M University System, Amarillo 79106.

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Accepted for publication 25 September 2009.

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.

Additional keywords:Beet soilborne mosaic virus, Benyvirus, convergent evolution, rhizomania.

© 2010 The American Phytopathological Society