Genetic dissection of systemic acquired resistance
1Developmental, Cell and Molecular Biology Group, Department of Biology, LSRC Building, P. O. Box 91000, Duke University, Durham, North Carolina 27708-1000, USA. xdong@duke.edu
Abstract:
Significant progress has been made in the past year in understanding the mechanism of systemic acquired resistance. Mitogen-activated protein kinase cascades have been implicated as negative regulators of salicyclic acid accumulation and the induction of resistance. The salicylic acid signal is transduced through NPR1, a nuclear-localized protein that interacts with transcription factors that are involved in regulating salicylic-acid-mediated gene expression. Both promoter analyses and genetic studies have shown that gene expression in systemic acquired resistance requires not only the activation of a transcriptional activator(s) but also inhibition of a transcriptional repressor(s). Microarray experiments have been performed to search for those genes whose expression is transcriptionally regulated during systemic acquired resistance and to identify common promoter elements that control these genes.
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