Journal of Microbiology

Research Support, Non-U.S. Gov'ts

The Use of Pseudomonas fluorescens P13 to Control Sclerotinia Stem Rot (Sclerotinia sclerotiorum) of Oilseed Rape: Hui Li , Huaibo Li , Yan Bai , Jing Wang , Ming Nie , Bo Li , Ming Xiao; J. Microbiol. 2011;49(6):884-889. Published online December 28, 2011; DOI: https://doi.org/10.1007/s12275-011-1261-4

Abstract: Sclerotinia stem rot (SSR) caused by the fungus Sclerotinia sclerotiorum has been an increasing threat to oilseed rape (Brassica napus L.) cultivation. Efficient and environment‐friendly treatments are much needed. Here we focus on microbial control. The Pseudomonas fluorescens P13 that was isolated from oilseed rape cultivation soil, proved to be a useful biocontrol strain for application. Morphology, physiological and biochemical tests and 16S rDNA analysis demonstrated that it was P. fluorescens P13 and that it had a broad antagonistic spectrum, significantly lessening the mycelial growth of S. sclerotiorum by 84.4% and suppressing sclerotial formation by 95‐100%. Scanning electron microscopy studies attested that P13 deformed S. sclerotiorum mycelia when they were cultured together. P13 did not produce chitinase but did produce hydrogen cyanide (HCN) which was likely one of the antagonistic mechanisms. The density of P13 remained at a high level (≥106 CFU/ml) during 5 weeks in the rhizosphere soil and roots. P13 reduced SSR severity at least by 59% in field studies and also promoted seedling growth (p<0.05) at the seedling stage. From these data, our work provided evidence that P13 could be a good alternative biological resource for biocontrol of S. sclerotiorum.

Molecular Analysis of the Copper-Responsive CopRSCD of a Pathogenic Pseudomonas fluorescens Strain: Yong-hua Hu , Hua-lei Wang , Min Zhang , Li Sun; J. Microbiol. 2009;47(3):277-286. Published online June 26, 2009; DOI: https://doi.org/10.1007/s12275-008-0278-9

Abstract: CopRS/CopABCD is one of the known systems that control copper homeostasis in bacteria. Although CopRS/CopABCD homologues are found to exist in Pseudomonas fluorescens, the potential role of this system in P. fluorescens has not been investigated. In this study a genetic cluster, consisting of copR, S, C, and D but lacking copAB, was identified in a pathogenic P. fluorescens strain (TSS) isolated from diseased fish. The copRSCD cluster was demonstrated to be required for full copper resistance and regulated at the transcription level by Cu. Expression of copCD is regulated directly by the two-component response regulator CopR, which also regulates its own expression. Interruption of the regulated expression of copR affected bacterial growth, biofilm formation, and tissue dissemination and survival. A mutant CopR, which lacks the N-terminal signal receiver domain and is constitutively active, was found to have an attenuating effect on bacterial virulence when expressed in TSS. To our knowledge, this is the first report that suggests a link between CopR and bacterial pathogenicity in P. fluorescens.

Physical Analysis of nahQ and tnpA Genes from Pseudomonas fluorescens: Ja-Young Seol , Soon-Young Choi , Kyung Hee Min; J. Microbiol. 2001;39(4):338-342.

Abstract: Pseudomonas fluorescens SM11 is a naphthalene-degrading strain whose dissimilatory genes are chromosomally encoded. We have cloned the 2.9 kb Sal I fragment harboring genes for the naphthalene-degradation upper pathway. The nucleotide sequences were determined to be nahQ, tnpA, and partial regions of nahE genes. The nahQ encodes a protein of 188 amino acid residues with a deduced molecular weight of 20.8 kDa. The high homology with other proteins suggests that NahQ may be an active and useful protein which gives a selective advantage to naphthalene degradation. Transposase(TnpA) encodes a polypeptide chain with a molecular mass of 41.8 kDa consisting of 376 amino acid residues. The deduced anino acid sequence of tnpA revealed 96% idenitity with putative transposase of P. stutzeri OX1. It was assumed that transposase plays an important role in the evolution of the catabolic-pathway in the regulation of nah expression.

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