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Applied and Environmental Microbiology, March 2004, p. 1836-1842, Vol. 70, No. 3
0099-2240/04/$08.00+0 DOI: 10.1128/AEM.70.3.1836-1842.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Swiss Federal Research Institute for Fruit Production, Viticulture and Horticulture, CH-8820 Wädenswil,1 Laboratoire de Biologie Microbienne, Université de Lausanne, CH-1015 Lausanne,2 Institut für Pflanzenwissenschaften, Phytomedizin/Phytopathologie, Eidgenössiche Technische Hochschule, CH-8092 Zürich, Switzerland3
Received 18 November 2002/ Accepted 25 November 2003
Multitrophic interactions mediate the ability of fungal pathogens to cause plant disease and the ability of bacterial antagonists to suppress disease. Antibiotic production by antagonists, which contributes to disease suppression, is known to be modulated by abiotic and host plant environmental conditions. Here, we demonstrate that a pathogen metabolite functions as a negative signal for bacterial antibiotic biosynthesis, which can determine the relative importance of biological control mechanisms available to antagonists and which may also influence fungus-bacterium ecological interactions. We found that production of the polyketide antibiotic 2,4-diacetylphloroglucinol (DAPG) was the primary biocontrol mechanism of Pseudomonas fluorescens strain Q2-87 against Fusarium oxysporum f. sp. radicis-lycopersici on the tomato as determined with mutational analysis. In contrast, DAPG was not important for the less-disease-suppressive strain CHA0. This was explained by differential sensitivity of the bacteria to fusaric acid, a pathogen phyto- and mycotoxin that specifically blocked DAPG biosynthesis in strain CHA0 but not in strain Q2-87. In CHA0, hydrogen cyanide, a biocide not repressed by fusaric acid, played a more important role in disease suppression.
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