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Higher Copy Numbers of the Potato RB Transgene Correspond to Enhanced Transcript and Late Blight Resistance Levels

April 2009 , Volume 22 , Number  4
Pages  437 - 446

James M. Bradeen,1 Massimo Iorizzo,1,2 Dimitre S. Mollov,1 John Raasch,3 Lara Colton Kramer,4 Benjamin P. Millett,1 Sandra Austin-Phillips,3 Jiming Jiang,4 and Domenico Carputo2

1University of Minnesota, Department of Plant Pathology, 495 Borlaug Hall, 1991 Upper Buford Circle, St. Paul, MN 55108, U.S.A.; 2University of Naples “Federico II”, Department of Soil, Plant, Environmental and Animal Production Sciences, Via Universitá 100-80055, Portici, Italy; 3University of Wisconsin, Biotechnology Center, 425 Henry Mall, Madison, WI 53706, U.S.A.; 4University of Wisconsin, Department of Horticulture, 1575 Linden Drive, Madison, WI 53706, U.S.A.


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Accepted 20 December 2008.

Late blight of potato ranks among the costliest of crop diseases worldwide. Host resistance offers the best means for controlling late blight, but previously deployed single resistance genes have been short-lived in their effectiveness. The foliar blight resistance gene RB, previously cloned from the wild potato Solanum bulbocastanum, has proven effective in greenhouse tests of transgenic cultivated potato. In this study, we examined the effects of the RB transgene on foliar late blight resistance in transgenic cultivated potato under field production conditions. In a two-year replicated trial, the RB transgene, under the control of its endogenous promoter, provided effective disease resistance in various genetic backgrounds, including commercially prominent potato cultivars, without fungicides. RB copy numbers and transcript levels were estimated with transgene-specific assays. Disease resistance was enhanced as copy numbers and transcript levels increased. The RB gene, like many other disease resistance genes, is constitutively transcribed at low levels. Transgenic potato lines with an estimated 15 copies of the RB transgene maintain high RB transcript levels and were ranked among the most resistant of 57 lines tested. We conclude that even in these ultra--high copy number lines, innate RNA silencing mechanisms have not been fully activated. Our findings suggest resistance-gene transcript levels may have to surpass a threshold before triggering RNA silencing. Strategies for the deployment of RB are discussed in light of the current research.



© 2009 The American Phytopathological Society