August
2011
, Volume
101
, Number
8
Pages
996
-
1,004
Authors
Jolien D'aes,
Gia Khuong Hoang Hua,
Katrien De Maeyer,
Joke Pannecoucque,
Ilse Forrez,
Marc Ongena,
Lars E. P. Dietrich,
Linda S. Thomashow,
Dmitri V. Mavrodi, and
Monica Höfte
Affiliations
First, second, third, fourth, and tenth authors: Laboratory of Phytopathology, Faculty of Bioscience Engineering, and fifth author: Laboratory of Microbial Ecology and Technology, Faculty of Bioscience Engineering, Ghent University, Coupure Links, 653, B-9000 Gent, Belgium; sixth author: Gembloux Agro-Bio Tech, University of Liege, Passage des Déportés, 2, B-5030 Gembloux, Belgium; seventh author: Department of Biological Sciences, Fairchild Center, 1108, Columbia University, New York 10027; eighth author: USDA-ARS, Root Disease and Biological Control Research Unit, Washington State University, Pullman 99164-6430; and ninth author: Department of Plant Pathology, Washington State University, Johnson Hall, 365, Pullman 99164-6430.
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RelatedArticle
Accepted for publication 3 March 2011.
Abstract
ABSTRACT
Pseudomonas CMR12a was previously selected as an efficient biocontrol strain producing phenazines and cyclic lipopeptides (CLPs). In this study, biocontrol capacity of Pseudomonas CMR12a against Rhizoctonia root rot of bean and the involvement of phenazines and CLPs in this ability were tested. Two different anastomosis groups (AGs) of Rhizoctonia solani, the intermediately aggressive AG 2-2 and the highly aggressive AG 4 HGI, were included in growth-chamber experiments with bean plants. The wild-type strain CMR12a dramatically reduced disease severity caused by both R. solani AGs. A CLP-deficient and a phenazine-deficient mutant of CMR12a still protected bean plants, albeit to a lesser extent compared with the wild type. Two mutants deficient in both phenazine and CLP production completely lost their biocontrol activity. Disease-suppressive capacity of CMR12a decreased after washing bacteria before application to soil and thereby removing metabolites produced during growth on plate. In addition, microscopic observations revealed pronounced branching of hyphal tips of both R. solani AGs in the presence of CMR12a. More branched and denser mycelium was also observed for the phenazine-deficient mutant; however, neither the CLP-deficient mutant nor the mutants deficient in both CLPs and phenazines influenced hyphal growth. Together, results demonstrate the involvement of phenazines and CLPs during Pseudomonas CMR12a-mediated biocontrol of Rhizoctonia root rot of bean.
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© 2011 The American Phytopathological Society