|Caldo, Rico - IOWA STATE UNIVERSITY|
|Nettleton, Dan - IOWA STATE UNIVERSITY|
Submitted to: Society for In Vitro Biology Proceedings
Publication Type: Proceedings
Publication Acceptance Date: April 28, 2005
Publication Date: June 3, 2005
Citation: Caldo, R.A., Nettleton, D., Wise, R.P. 2005. Interplay of gene-specific disease resistance, basal defense, and the suppression of host-responses. 2005 Society for In Vitro Biology Proceedings. PS1. 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. To ascertain the global framework of host gene expression during biotrophic pathogen invasion, we have utilized the 22K Barley1 GeneChip to analyze the transcriptional regulation of 22,792 host genes throughout various interactions among barley and the powdery mildew fungus, Blumeria graminis f. sp. hordei (Bgh). Near-isogenic barley lines with introgressed Mla CC-NBS-LRR resistance alleles and associated mutants were utilized to identify genes with significant differential expression in incompatible and compatible interactions. Using linear mixed model analyses, over 50 genes exhibited highly similar patterns of upregulation among all incompatible and compatible interactions up to 16 hours after inoculation (hai), coinciding with germination of Bgh conidiospores and formation of appressoria. By 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. Based on these results, we propose a model that links the recognition of general elicitors and specific avirulence proteins in the expression of plant defense responses, supporting the hypothesis that host-specific resistance evolved from the recognition and prevention of the pathogen’s suppression of plant basal defense.