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Lr34-Mediated Leaf Rust Resistance in Wheat: Transcript Profiling Reveals a High Energetic Demand Supported by Transient Recruitment of Multiple Metabolic Pathways

December 2008 , Volume 21 , Number  12
Pages  1,515 - 1,527

Melvin D. Bolton,1 James A. Kolmer,2 Wayne W. Xu,3 and David F. Garvin1

1United States Department of Agriculture--Agricultural Research Service (USDA-ARS), Plant Science Research Unit, 411 Borlaug Hall, University of Minnesota, 1991 Upper Buford Circle, St. Paul 55108, U.S.A.; 2USDA-ARS, Cereal Disease Laboratory, 1551 Lindig St., University of Minnesota, St. Paul 55108, U.S.A.; 3Supercomputing Institute, 550 Walter Library, 117 Pleasant Street SE, University of Minnesota, Minneapolis 55455, U.S.A.

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Accepted 18 August 2008.

The wheat gene Lr34 confers partial resistance to all races of Puccinia triticina, the causal agent of wheat leaf rust. However, the biological basis for the exceptional durability of Lr34 is unclear. We used the Affymetrix GeneChip Wheat Genome Array to compare transcriptional changes of near-isogenic lines of Thatcher wheat in a compatible interaction, an incompatible interaction conferred by the resistance gene Lr1, and the race-nonspecific response conditioned by Lr34 3 and 7 days postinoculation (dpi) with P. triticina. No differentially expressed genes were detected in Lr1 plants at either timepoint whereas, in the compatible Thatcher interaction, differentially expressed genes were detected only at 7 dpi. In contrast, differentially expressed genes were identified at both timepoints in P. triticina-inoculated Lr34 plants. At 3 dpi, upregulated genes associated with Lr34-mediated resistance encoded various defense and stress-related proteins, secondary metabolism enzymes, and transcriptional regulation and cellular-signaling proteins. Further, coordinated upregulation of key genes in several metabolic pathways that can contribute to increased carbon flux through the tricarboxylic cycle was detected. This indicates that Lr34-mediated resistance imposes a high energetic demand that leads to the induction of multiple metabolic responses to support cellular energy requirements. These metabolic responses were not sustained through 7 dpi, and may explain why Lr34 fails to inhibit the pathogen fully but does increase the latent period.

Additional keywords:β-oxidation, GABA, gene expression, glycolysis, PDH bypass, TCA cycle.

The American Phytopathological Society, 2008