Mechanisms of antagonism of Pseudomonas fluorescens EPS62e against Erwinia amylovora, the causal agent of fire blight Autores/as Jordi Cabrefiga Institute of Food and Agricultural Technology-CIDSAV, University of Girona, Girona, Spain Anna Bonaterra Institute of Food and Agricultural Technology-CIDSAV, University of Girona, Girona, Spain Emilio Montesinos Institute of Food and Agricultural Technology-CIDSAV, University of Girona, Girona, Spain Palabras clave: Erwinia amylovora, Pseudomonas fluorescens, fire blight disease, biological antagonism Resumen Pseudomonas fluorescens EPS62e was selected during a screening procedure for its high efficacy in controlling infections by Erwinia amylovora, the causal agent of fire blight disease, on different plant materials. In field trials carried out in pear trees during bloom, EPS62e colonized flowers until the carrying capacity, providing a moderate efficacy of fire-blight control. The putative mechanisms of EPS62e antagonism against E. amylovora were studied. EPS62e did not produce antimicrobial compounds described in P. fluorescens species and only developed antagonism in King’s B medium, where it produced siderophores. Interaction experiments in culture plate wells including a membrane filter, which physically separated the cultures, confirmed that inhibition of E. amylovora requires cell-to-cell contact. The spectrum of nutrient assimilation indicated that EPS62e used significantly more or different carbon sources than the pathogen. The maximum growth rate and affinity for nutrients in immature fruit extract were higher in EPS62e than in E. amylovora, but the cell yield was similar. The fitness of EPS62e and E. amylovora was studied upon inoculation in immature pear fruit wounds and hypanthia of intact flowers under controlled-environment conditions. When inoculated separately, EPS62e grew faster in flowers, whereas E. amylovora grew faster in fruit wounds because of its rapid spread to adjacent tissues. However, in preventive inoculations of EPS62e, subsequent growth of EPS101 was significantly inhibited. It is concluded that cell-to-cell interference as well as differences in growth potential and the spectrum and efficiency of nutrient use are mechanisms of antagonism of EPS62e against E. amylovora. [Int Microbiol 2007; 10(2):123-132] Biografía del autor/a Jordi Cabrefiga, Institute of Food and Agricultural Technology-CIDSAV, University of Girona, Girona, Spain Institute of Food and Agricultural Technology-CIDSAV, University of Girona, Girona, Spain Anna Bonaterra, Institute of Food and Agricultural Technology-CIDSAV, University of Girona, Girona, Spain Institute of Food and Agricultural Technology-CIDSAV, University of Girona, Girona, Spain Emilio Montesinos, Institute of Food and Agricultural Technology-CIDSAV, University of Girona, Girona, Spain Institute of Food and Agricultural Technology-CIDSAV, University of Girona, Girona, Spain Descargas PDF (English) Publicado 2010-01-26 Número Vol. 10 Núm. 2 (2007) Sección Research Articles Licencia Submission of a manuscript to International Microbiology implies: that the work described has not been published before, including publication in the World Wide Web (except in the form of an Abstract or as part of a published lecture, review, or thesis); that it is not under consideration for publication elsewhere; that all the coauthors have agreed to its publication. The corresponding author signs for and accepts responsability for releasing this material and will act on behalf of any and all coauthors regarding the editorial review and publication process.If an article is accepted for publication in International Microbiology, the authors (or other copyright holder) must transfer to the journal the right–not exclusive–to reproduce and distribute the article including reprints, translations, photographic reproductions, microform, electronic form (offline, online) or any other reproductions of similar nature. Nevertheless, all article in International Microbiology will be available on the Internet to any reader at no cost. The journal allows users to freely download, copy, print, distribute, search, and link to the full text of any article, provided the authorship and source of the published article is cited. The copyright owner's consent does not include copying for new works, or resale. In these cases, the specific written permission of International Microbiology must first be obtained.Authors are requested to create a link to the published article on the journal's website. The link must be accompanied by the following text: "The original publication is available on LINK at <http://www.im.microbios.org>. Please use the appropiate URL for the article in LINK. Articles disseminated via LINK are indexed, abstracted, and referenced by many abstracting and information services, bibliographic networks, subscription agencies, library networks, and consortia.