Submitted to: International Plant Growth Promoting Rhizobacteria Workshop
Publication Type: Abstract Only
Publication Acceptance Date: April 15, 2009
Publication Date: May 17, 2009
Citation: Kidarsa, T.A., Loper, J.E. 2009. Microarray analysis of Pseudomonas fluorescens Pf-5 grown onseed surfaces. International Plant Growth Promoting Rhizobacteria Workshop. p. 24. Technical Abstract: The biological control agent Pseudomonas fluorescens Pf-5 suppresses seedling emergence diseases caused by soilborne fungi and Oomycetes. Genes expressed by a biological control agent on seed surfaces determine the outcome of its interaction with target pathogens in the spermosphere, the soil surrounding seed surfaces. Seed exudates provide nutrition for both the biological control agent and the pathogen and can trigger germination and growth of pathogenic propagules. In addition, exudates may influence the spectrum of secondary metabolites produced by the biological control organism, thereby affecting its efficacy. To better understand mechanisms of biological control in the spermosphere, we performed microarray analysis of Pf-5 grown on pea seeds, comparing the transcriptional response of wild-type Pf-5 and derivative strains carrying a mutation in one of the regulatory genes gacA or rpoS. The gacS/gacA two-component regulatory system is required for secondary metabolite production in Pf-5 and gacS or gacA mutations lead to reduced biological control efficacy in many strains of Pseudomonas. In contrast, mutations in the sigma factor rpoS can enhance biological control of seedling diseases caused by the Oomycete Pythium ultimum. Genes downregulated in the gacA mutant include genes for biosynthesis of the secondary metabolites, 2,4-diacetylphloroglucinol, pyrrolnitrin, orfamide A, and rhizoxin analogs and genes encoding a type VI secretion system. Genes involved in iron acquisition were upregulated in the gacA mutant. Pyrrolnitrin and rhizoxin biosynthetic genes were also downregulated in the rpoS mutant, while pyoluteorin and 2,4-diacetylphloroglucinol genes were upregulated.