Submitted to: American Society of Plant Biologists Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: May 1, 2010
Publication Date: May 1, 2010
Citation: Okubara, P.A. 2010. Cultivar-dependent root colonization, antifungal metabolite accumulation and gene expression in the wheat-Pseudomonas interaction. American Society of Plant Biologists Annual Meeting. Pullman, WA May 1, 2010, p.5. Technical Abstract: We explored the role of host genotype in three aspects of the wheat-Pseudomonas biocontrol interaction: rhizosphere population density, accumulation of rhizosphere 2,4-diacetylphloroglucinol (DAPG), and Pseudomonas-mediated changes in root gene expression. Wheat cultivars varied in ability to support P. fluorescens strain Q8r1-96, an aggressive and persistent colonizer, compared to strain Q2-87, a moderately aggressive, less persistent colonizer. Of 27 cultivars tested, Finley and six others supported significantly (P<0.05) higher rhizosphere populations of Q8r1-96 than Q2-87 after 14 d in a non-pasteurized, non-agricultural soil. Cultivar Tara supported relatively high population densities of both bacterial strains, whereas Buchanan supported low population densities of both strains. In a soil-free system, roots of cultivars Tara and Finley accumulated more DAPG when colonized by Q8r1-96 compared to Q2-87. In contrast, Buchanan accumulated the same amounts of DAPG during colonization by both strains, even though Q8r1-96 produced about 100-fold more metabolite than Q2-87 in King’s Medium B. These findings demonstrated that rhizoplane DAPG accumulation, like rhizosphere population density, is dependent upon a cultivar-bacterial strain interaction. Cultivar-dependent responses to rhizobacteria were also noted at the gene expression level. In microarray experiments, genes were differentially up- or down-regulated in wheat near-isogenic lines 442, 443 and in cv. Finley in response to root colonization by Q8r1-96. Real-time PCR was used to validate transcriptional changes in 16 genes involved in general stress response and basal resistance, including COI1, PR-10a, Avr9-2, HRin1 and HRin2.