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Title:   Author  item
                                            Wise, Rogeritem
                                            CALDO, RICO - IOWA STATE UNIVERSITYitem
                                            Halterman, Dennisitem
                                            NETTLETON, DAN - IOWA STATE UNIVERSITY
  Submitted to: Cereal Rusts and Mildews Conference European and Mediterranean  Proceedings
                                    Publication Type: Proceedings
                                    Publication Acceptance Date: 7/6/2004
                                    Publication  Date: 8/22/2004
                                    Citation: Wise, R.P., Caldo, R.A., Halterman, D.A., Nettleton, D.A. 2004. Flor revisited: Systems biology in barley-powdery mildew interactions. Cereal Rusts and Mildews Conference European and Mediterranean Proceedings. Abstract 1.14, Cereal Rusts and Powdery Mildews Bulletin.Interpretive Summary:
                                Technical Abstract: Active plant defense to microbial attack is highly dependent upon recognition events involving associated gene products in the host and the pathogen.  Both perception of general and specific pathogen-associated molecules result in signal transduction cascades ultimately leading to disease resistance.  General elicitors, which include proteins, glycoproteins, peptides, carbohydrates and lipids, signal the presence of the pathogen and are able to trigger defense responses in a non-cultivar specific manner.  In contrast, specific effectors, encoded by pathogen avirulence genes, trigger cultivar-specific responses resulting in hyperactivation of basal defense, which is often accompanied by hypersensitive cell death.  This specific recognition in plant-pathogen interactions conforms to the gene-for-gene hypothesis and is determined by direct or indirect interaction of host resistance (R) proteins and cognate pathogen-derived avirulence (AVR) effectors.  Although many studies have been conducted on plant perception of pathogen-derived molecules, the link between the recognition of general and specific elicitors in the expression of compatibility and incompatibility responses remains poorly understood.

To ascertain the global framework of host gene expression during biotrophic pathogen invasion, we analyzed in parallel the mRNA abundance of 22,792 host genes throughout 36 (genotype x pathogen x time) interactions between barley (Hordeum vulgare) and Blumeria graminis f. sp. hordei (Bgh), the causal agent of powdery mildew disease.  A split-split-plot design was used to investigate near-isogenic barley lines with introgressed Mla6, Mla13, and Mla1 CC-NBS-LRR resistance alleles challenged with Bgh isolates 5874 (AvrMla6, AvrMla1) and K1 (AvrMla13, AvrMla1).  A linear mixed model analysis was employed to identify genes with significant differential expression (p-value<0.0001) in incompatible and compatible barley-Bgh interactions across six time points after pathogen challenge.  Twenty-two host genes, of which five were of unknown function, exhibited highly similar patterns of up-regulation among all incompatible and compatible interactions up to 16 hours after inoculation (hai), coinciding with germination of Bgh conidiospores and formation of appressoria.  In contrast, significant divergent expression was observed from 16 to 32 hai, during membrane-to-membrane contact between fungal haustoria and host epidermal cells, with notable suppression of most transcripts identified as differentially expressed in compatible interactions.  These findings provide a link between the recognition of general and specific pathogen-associated molecules in gene-for-gene specified resistance and support the hypothesis that host-specific resistance evolved from the recognition and prevention of the pathogen's suppression of plant basal defense.
Research supported by USDA Initiative for Future Agriculture and Food Systems (IFAFS) grant no. 2001-52100-11346, USDA National Research Initiative (NRI) grant no. 02-35300-12619, and the USDA-CSREES North American Barley Genome Project.


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