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Title

From the root to the stem: Interaction between the biocontrol root endophyte Pseudomonas fluorescensPICF7 and the pathogen Pseudomonas savastanoi NCPPB 3335 in olive knots

AuthorsMaldonado-González, María Mercedes ; Prieto, Pilar ; Ramos, Cayo; Mercado-Blanco, Jesús
Issue DateMay-2013
PublisherWiley-Blackwell
CitationMicrobial Biotechnology 6(3): 275-287 (2013)
AbstractOlive knot disease, caused by Pseudomonas savastanoi pv. savastanoi, is one of the most important biotic constraints for olive cultivation. Pseudomonas fluorescensPICF7, a natural colonizer of olive roots and effective biological control agent (BCA) against Verticillium wilt of olive, was examined as potential BCA against olive knot disease. Bioassays using in vitro-propagated olive plants were carried out to assess whether strain PICF7 controlled knot development either when co-inoculated with the pathogen in stems or when the BCA (in roots) and the pathogen (in stems) were spatially separated. Results showed that PICF7 was able to establish and persist in stem tissues upon artificial inoculation. While PICF7 was not able to suppress disease development, its presence transiently decreased pathogen population size, produced less necrotic tumours, and sharply altered the localization of the pathogen in the hyperplasic tissue, which may pose epidemiological consequences. Confocal laser scanning microscopy combined with fluorescent tagging of bacteria revealed that when PICF7 was absent the pathogen tended to be localized at the knot surface. However, presence of the BCA seemed to confine P. savastanoi at inner regions of the tumours. This approach has also enabled to prove that the pathogen can moved systemically beyond the hypertrophied tissue. Pseudomonas fluorescens PICF7, a natural colonizer of olive roots and effective biological control agent (BCA) against Verticillium wilt of olive, was examined as potential BCA against olive knot disease caused by Pseudomonas savastanoi pv. savastanoi. While PICF7 was not able to suppress disease development, its presence transiently decreased pathogen population size, produced less necrotic tumors, and sharply altered the localization of the pathogen in the hyperplasic tissue. Confocal laser scanning microscopy revealed that when PICF7 was absent the pathogen tended to be localized at the knot surface. However, presence of the BCA seemed to confine P. savastanoi at inner regions of the tumors. This approach has also enabled to prove that the pathogen can moved systemically beyond the hypertrophied tissue. © 2013 The Authors. Published by Society for Applied Microbiology and Blackwell Publishing Ltd.
Publisher version (URL)http://dx.doi.org/10.1111/1751-7915.12036
URIhttp://hdl.handle.net/10261/94998
DOI10.1111/1751-7915.12036
Identifiersdoi: 10.1111/1751-7915.12036
issn: 1751-7907
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