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Title:   Author  item
                                            FOSTER-HARTNETT, D - UNIVERSITY OF MINNESOTAitem
                                            DANESH, D - UNIVERSITY OF MINNESOTAitem
                                            PENUELA, S - UNIVERSITY OF MINNESOTAitem
                                            SHAROPOVA, N - UNIVERSITY OF MINNESOTAitem
                                            VANDENBOSCH, K - UNIVERSITY OF MINNESOTAitem
                                            YOUNG, N - UNIVERSITY OF MINNESOTAitem
                                            Samac, Deborah

                                                         - *Debby*
  Submitted to: Meeting Abstract
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 6/5/2005
                                    Publication  Date: 6/5/2005
                                    Citation: Foster-Hartnett, D., Danesh, D., Penuela, S., Sharopova, N., VandenBosch, K.A., Young, N.D., Samac, D.A. 2005. Using microarray analysis to identify genes associated with basal resistance and the hypersensitive response (HR) in Medicago truncatula [abstract]. 2005 Model Legume Congress, June 5-9, 2005, Pacific Grove, California. Abstract No. P54.Interpretive Summary:
                                Technical Abstract: Powdery mildew of pea and anthracnose of alfalfa are two economically important diseases of legumes. We have identified a range of disease phenotypes by screening M. truncatula accessions with the causal agents of powdery mildew and anthracnose, the biotrophic fungus Erysiphe pisi, and the hemibiotrophic/necrotrophic fungus Colletotrichum trifolii. Resistant genotypes responded to inoculation by producing H2O2 and fluorescent compounds at the pathogen penetration site, consistent with a hypersensitive response (HR). These observations combined with genetic data from our lab and others suggest R-gene mediated resistance mechanisms. We used 6K EST microarray chips to assess E. pisi- induced early transcriptional changes in highly resistant, moderately resistant, and susceptible genotypes and C. trifolii-induced changes in a resistant genotype. Genes that were similarly up- or down-regulated (54 total) in the four experimental groups were considered part of the basal disease response. These included pathogenesis-related (PR) genes and others involved in defense signal transduction, senescence, cell wall metabolism, heat shock and dessication stresses. We also identified nine basal response genes with unknown function and/or low homology. Genes up- or down-regulated in two or three resistant interactions at least 2.5-fold greater than in the susceptible interaction were associated with the HR response (41 total). These included flavonoid/lignin pathway genes, a xyloglucan-specific fungal endoglucanase inhibitor, a phospholipase A2, a ubiquitin-protein ligase, and several others involved in transport, transcription regulation, and signal transduction. Seventeen unknown genes, including at least one that is legume-specific, were up-regulated in resistant genotypes. We also assessed the similarity between the HR responses to E. pisi and C. trifolii. Very few genes were uniquely up-regulated during the C. trifolii infection (3% total) or the E. pisi infection (14%). Therefore, the early resistance response to two different pathogens appears to be quite similar. Finally, we took advantage of the M. truncatula genome sequencing project by analyzing promoter sequences of coordinately regulated genes. In the up-regulated set, we found statistically significant levels of four transcription factor binding sites previously associated with the defense response. In the down-regulated set, we found two highly conserved, novel motifs that may be involved in pathogen-induced gene repression.


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