Open AccessPhenazines are not essential for Pseudomonas chlororaphis PA23 biocontrol of Sclerotinia sclerotiorum , but do play a role in biofilm formation
Author(s) -
Selin Carrie,
Habibian Rahim,
Poritsanos Nicole,
Athukorala Sarangi N.P.,
Fernando Dilantha,
De Kievit Teresa R.
Publication year - 2010
Publication title -
fems microbiology ecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.377
H-Index - 155
eISSN - 1574-6941
pISSN - 0168-6496
DOI - 10.1111/j.1574-6941.2009.00792.x
Subject(s) - pseudomonas chlororaphis , sclerotinia sclerotiorum , biology , microbiology and biotechnology , pathogen , sclerotinia , biofilm , botrytis cinerea , bacteria , mutant , pseudomonas , biochemistry , botany , gene , genetics
Abstract Pseudomonas chlororaphis strain PA23 is a biocontrol agent capable of suppressing disease caused by the fungal pathogen Sclerotinia sclerotiorum . This bacterium produces the diffusible antibiotics phenazine‐1‐carboxylic acid, 2‐hydroxyphenazine and pyrrolnitrin (PRN). Because the individual contribution of these antibiotics to PA23 biocontrol has not been defined, mutants deficient in the production of phenazine (PHZ), PRN or both antibiotics were created. Analysis of the PHZ mutant revealed enhanced antifungal activity in vitro and wild‐type levels of Sclerotinia disease suppression. Conversely, the PRN‐ and the PRN/PHZ‐deficient strains exhibited decreased antifungal activity in vitro and markedly reduced the ability to control Sclerotinia infection of canola in the greenhouse. These findings suggest that PRN is the primary antibiotic mediating biocontrol of this pathogen. Analysis of prnA–lacZ and phzA–lacZ transcriptional fusions revealed that PRN and PHZ are not subject to autoregulation; moreover, they do not cross‐regulate each other. However, HPLC showed a twofold increase in PRN levels in the PHZ − background. Finally, PHZ, but not PRN production, is involved in biofilm development in P. chlororaphis PA23.