Matthew J. Moscou,1,2
Rico A. Caldo,2
Dan Nettleton,1,4 and
Roger P. Wise1,2,3
1Interdepartmental Program in Bioinformatics and Computational Biology, and 2Department of Plant Pathology, Iowa State University, Ames, IA 50011-1020, U.S.A.; 3Corn Insects and Crop Genetics Research Unit, USDA-ARS, Ames, IA 50011-1020, U.S.A.; 4Department of Statistics, Iowa State University, Ames, IA 50011-1210, U.S.A.
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Accepted 6 February 2011.
Barley Mildew resistance locus a (Mla) is a major determinant of immunity to the powdery mildew pathogen, Blumeria graminis f. sp. hordei. Alleles of Mla encode cytoplasmic- and membrane-localized coiled-coil, nucleotide binding site, leucine-rich repeat proteins that mediate resistance when complementary avirulence effectors (AVRa) are present in the pathogen. Presence of an appropriate AVRa protein triggers nuclear relocalization of MLA, in which MLA binds repressing host transcription factors. Timecourse expression profiles of plants harboring Mla1, Mla6, and Mla12 wild-type alleles versus paired loss-of-function mutants were compared to discover conserved transcriptional targets of MLA and downstream signaling cascades. Pathogen-dependent gene expression was equivalent or stronger in susceptible plants at 20 h after inoculation (HAI) and was attenuated at later timepoints, whereas resistant plants exhibited a time-dependent strengthening of the transcriptional response, increasing in both fold change and the number of genes differentially expressed. Deregulation at 20 HAI implicated 16 HAI as a crucial point in determining the future trajectory of this interaction and was interrogated by quantitative analysis. In total, 28 potential transcriptional targets of the MLA regulon were identified. These candidate targets possess a diverse set of predicted functions, suggesting that multiple pathways are required to mediate the hypersensitive reaction.
This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 2011.