|D'AES, JOLIEN - Ghent University|
|KHUONG, HOANG HUA - Ghent University|
|DE MAEYER, KATRIEN - Ghent University|
|PANNECOUCQUE, JOKE - Ghent University|
|FORREZ, ILSE - Ghent University|
|ONGENA, MARC - University Of Liege|
|DIETRICH, LARS - Columbia University|
|MAVRODI, DMITRI - Washington State University|
|MAVRODI, OLGA - Washington State University|
|HOFTE, MONICA - Ghent University|
Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/3/2011
Publication Date: 3/3/2011
Citation: D'Aes, J., Khuong, H.G., De Maeyer, K., Pannecoucque, J., Forrez, I., Ongena, M., Dietrich, L.E., Thomashow, L.S., Mavrodi, D.V., Mavrodi, O.V., Hofte, M. 2011. Biological control of Rhizoctonia root rot on bean by phenazine- and cyclic lipopeptide-producing Pseudomonas CMR12a. Phytopathology. 101(8):996-1004.
Interpretive Summary: The bacterial biological control strain CMR12a controls the soilborne disease Rhizoctonia root rot of bean and produces two kinds of compounds, phenazines and cyclic lipoproteins (CLPs), that are known to contribute to disease control by other bacteria. In this study, mutants deficient in the CLPs, the phenazines, or both kinds of compounds were created and tested for the ability to control Rhizoctonia root rot. Mutants deficient in either CLPs or phenazines still protected the bean plants against the pathogen, but to a lesser extent than the parental strain. However, mutants deficient in both kinds of compounds completely lost their ability to biocontrol activity. These results show that both kinds of compounds contribute to the protective effects of CMR12a.
Technical 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 CMR12amediated biocontrol of Rhizoctonia root rot of bean.