|Caldo, Rico - IOWA STATE UNIVERSITY|
|Nettleton, Dan - IOWA STATE UNIVERSITY|
Submitted to: Biology of Plant Microbe Interactions
Publication Type: Book / Chapter
Publication Acceptance Date: December 19, 2005
Publication Date: October 28, 2006
Citation: Caldo, R.A., Nettleton, D., Wise, R.P. 2006. Interplay of gene-specific disease resistance, basal defense, and the suppression of host responses to barley powdery mildew. In: Sanchez, F., Quinto, C., Lopez-Lara, I., Geiger, O., editors. Biology of Plant Microbe Interactions. St. Paul, MN: International Society of Molecular Plant-Microbe Interactions. Vol. 5, p. 620-624. Technical Abstract: Major efforts have been devoted to understanding the mechanisms of genetic resistance and incorporating them into breeding programs to offset yield loss caused by pathogens. Historically, cereal crops have laid the foundation for numerous classical genetic studies in host-pathogen biology, resulting in many model biological systems. We have focused on the well-characterized, barley-powdery mildew pathosystem as our entry point to address fundamental questions regarding host resistance. In this system, resistance to the obligate biotroph, Blumeria graminis f. sp. hordei (Bgh), is governed by gene-for-gene-specified interactions of barley Ml genes and cognate powdery mildew avirulence (Avr) genes. A unique feature of this intricate biological system is that 92-97% similar CC-NBS-LRR proteins, encoded by Mla alleles, may or may not require RAR1, SGT1, and HSP90 as part of the SCF ubiquitin ligase complex to activate downstream components. To ascertain the global framework of host gene expression during biotrophic pathogen invasion, we utilized the Barley1 GeneChip to analyze the transcriptional regulation of 22,792 host genes throughout various time-course interactions among barley and the powdery mildew fungus, Blumeria graminis. Four-hundred thirty two Barley1 GeneChips, representing 144 replicated barley-powdery mildew interactions, were used to interrogate plants containing allelic variants and mutants of Mla, Rar1, and Rom1, a restorer of Rar1-independent, Mla12-specified resistance.