Inhibition of <i>Septoria tritici</i> and other phytopathogenic fungi and bacteria by <i>Pseudomonas fluorescens</i> and its antibiotics

Levy, Edna; Gough, F. J.; Berlin, K. Darrell; Guiana, P. W.; Smith, Jo

doi:10.1111/j.1365-3059.1992.tb02355.x

Cited by 73 publications

(34 citation statements)

References 17 publications

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“…This phenolic molecule has broad-spectrum antifungal (Levy et al, 1992;Schoonbeek et al, 2002;Tomas-Lorente et al, 1989;Weller & Cook, 1983), antibacterial (Levy et al, 1992), antihelminthic (Bowden et al, 1965; Harrison et al, 1993) and phytotoxic (Keel et al, 1992;Reddi et al, 1969) activities. PHL is the primary determinant of biological control by P. fluorescens F113 (Shanahan et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

The putative permease PhlE of Pseudomonas fluorescens F113 has a role in 2,4-diacetylphloroglucinol resistance and in general stress tolerance

et al. 2004

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2,4-Diacetylphloroglucinol (PHL) is the primary determinant of the biological control activity of Pseudomonas fluorescens F113. The operon phlACBD encodes enzymes responsible for PHL biosynthesis from intermediate metabolites. The phlE gene, which is located downstream of the phlACBD operon, encodes a putative permease suggested to be a member of the major facilitator superfamily with 12 transmembrane segments. PhlE has been suggested to function in PHL export. Here the sequencing of the phlE gene from P. fluorescens F113 and the construction of a phlE null mutant, F113-D3, is reported. It is shown that F113-D3 produced less PHL than F113. The ratio of cell-associated to free PHL was not significantly different between the strains, suggesting the existence of alternative transporters for PHL. The phlE mutant was, however, significantly more sensitive to high concentrations of added PHL, implicating PhlE in PHL resistance. Furthermore, the phlE mutant was more susceptible to osmotic, oxidative and heat-shock stresses. Osmotic stress induced rapid degradation of free PHL by the bacteria. Based on these results, we propose that the role of phlE in general stress tolerance is to export toxic intermediates of PHL degradation from the cells. INTRODUCTIONMany Pseudomonas fluorescens strains produce 2,4-diacetylphloroglucinol (PHL) (Bangera & Thomashow, 1996;Boruah & Kumar, 2002;Nowak-Thompson et al., 1994;Reddi & Borovkov, 1970; Sharifi-Tehrani et al., 1998). This phenolic molecule has broad-spectrum antifungal (Levy et al., 1992;Schoonbeek et al., 2002;Tomas-Lorente et al., 1989;Weller & Cook, 1983), antibacterial (Levy et al., 1992), antihelminthic (Bowden et al., 1965; Harrison et al., 1993) and phytotoxic (Keel et al., 1992;Reddi et al., 1969) activities. PHL is the primary determinant of biological control by P. fluorescens F113 (Shanahan et al., 1992). Synthesis of PHL is directed by the phlACBD genes, which are believed to constitute an operon (Bangera & Thomashow, 1996Delany, 1999). PhlD shows structural similarities with plant chalcone synthase, also called polyketide synthase type III, and is necessary but not sufficient for the synthesis of monoacetylphloroglucinol (MAPG) (Bangera & Thomashow, 1999). PhlA, PhlC and PhlB are necessary and sufficient for the transacetylation of MAPG to produce PHL (Bangera & Thomashow, 1999;Shanahan et al., 1992). The available data strongly suggest that PhlA, PhlC, PhlB and PhlD function in a multienzyme complex (Bangera & Thomashow, 1999;Delany, 1999). Expression of the phlACBD operon is subject to complex regulation (Aarons et al., 2000;Abbas et al., 2002;Bangera & Thomashow, 1999;Chou et al., 1993;Corbell & Loper, 1995;Delany, 1999; Delany et al., 2000;Duffy & Defago, 1999;Schnider-Keel et al., 2000). In addition, PHL is an autoregulator, positively influencing its own biosynthesis (Abbas et al., 2002;Schnider-Keel et al., 2000).Micro-organisms have developed various ways to resist the toxic effects of the secondary metabolites they produce. These mechanisms include expo...

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Section: Introductionmentioning

confidence: 99%

The putative permease PhlE of Pseudomonas fluorescens F113 has a role in 2,4-diacetylphloroglucinol resistance and in general stress tolerance

et al. 2004

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“…It has antifungal (28,55,58), antibacterial (28), antihelminthic (7,21), and phytotoxic (23,48) activities. PHL is a polyketide synthesized by condensation of three molecules of acetyl coenzyme A with one molecule of malonyl coenzyme A to produce the precursor monoacetylphloroglucinol, which is subsequently transacetylated to generate PHL (37,55).…”

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Characterization of Interactions between the Transcriptional Repressor PhlF and Its Binding Site at the phlA Promoter in Pseudomonas fluorescens F113

et al. 2002

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The phlACBD genes responsible for the biosynthesis of the antifungal metabolite 2,4-diacetylphloroglucinol (PHL) by the biocontrol strain Pseudomonas fluorescens F113 are regulated at the transcriptional level by the pathway-specific repressor PhlF. Strong evidence suggests that this regulation occurs mainly in the early logarithmic phase of growth. First, the expression of the phlF gene is relatively high between 3 and 13 h of growth and relatively low thereafter, with the phlACBD operon following an opposite expression profile. Second, the kinetics of PHL biosynthesis are specifically altered in the logarithmic phase in a P. fluorescens F113 phlF mutant. The phlA-phlF intergenic region presents a complex organization in that phlACBD is transcribed from a 70 RNA polymerase-dependent promoter that is likely to overlap the promoter of the divergently transcribed phlF gene. The repression by PhlF is due to its interaction with an inverted repeated sequence, phO, located downstream of the phlA transcriptional start site. Cross-linking experiments indicate that PhlF can dimerize in solution, and thus PhlF may bind phO as a dimer or higher-order complex. Furthermore, it is now demonstrated that certain regulators of PHL synthesis act by modulating PhlF binding to phO. PHL, which has previously been shown to be an autoinducer of PHL biosynthesis, interacts with PhlF to destabilize the PhlF-phO complex. Conversely, the PhlF-phO complex is stabilized by the presence of salicylate, which has been shown to be an inhibitor of phlA expression.2,4-Diacetylphloroglucinol (PHL) is a phenolic molecule produced by many fluorescent pseudomonad bacteria (3,23,42,47,55,56,61,63). It has antifungal (28, 55, 58), antibacterial (28), antihelminthic (7, 21), and phytotoxic (23, 48) activities. PHL is a polyketide synthesized by condensation of three molecules of acetyl coenzyme A with one molecule of malonyl coenzyme A to produce the precursor monoacetylphloroglucinol, which is subsequently transacetylated to generate PHL (37,55).The genes involved in the biosynthesis of PHL have been cloned and sequenced from a number of Pseudomonas strains (3,4,11,17,37,55,61). Genetic and sequence data show that the phl locus is comprised of a number of transcriptional units. The structural genes, phlA, phlC, phlB, and phlD, are transcribed as a single operon (phlACBD), with the putative permease gene, phlE, probably transcribed from its own promoter further downstream. The transcriptional repressor, phlF, is located upstream of the phlACBD operon and is transcribed in the opposite direction (4,11,54).

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“…Pf-5 produces the antifungal antibiotics pyrrolnitrin (8), pyoluteorin (9), and 2,4-diacetylphloroglucinol (Phl) (11). Each antibiotic has a unique spectrum of activity against fungal pathogens inhibited by Pf-5: pyrrolnitrin inhibits R. solani (8) and Pyrenophora triticirepentis (10), pyoluteorin inhibits Pythium ultimum (9), and Phl inhibits all three fungi (11)(12)(13) (15,16). A mutation in apdA or gacA of P. fluorescens abolishes the production of pyrrolnitrin, pyoluteorin, Phl, hydrogen cyanide, extracellular protease(s), and tryptophan side-chain oxidase (14)(15)(16).…”

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confidence: 99%

The sigma factor sigma s affects antibiotic production and biological control activity of Pseudomonas fluorescens Pf-5.

Sarniguet¹,

Kraus²,

Henkels³

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

198

199

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Pseudomonas fluorescens Pf-5, a rhizosphereinhabiting bacterium that suppresses several soilborne pathogens of plants, produces the antibiotics pyrrolnitrin, pyoluteorin, and 2,4-diacetylphloroglucinol. A gene necessary for pyrrolnitrin production by Pf-5 was identified as rpoS, which encodes the stationary-phase sigma factor as. Several pleiotropic effects of an rpoS mutation in Escherichia coli also were observed in an RpoS-mutant of Pf-5. These included sensitivities of stationary-phase cells to stresses imposed by hydrogen peroxide or high salt concentration. A plasmid containing the cloned wild-type rpoS gene restored pyrrolnitrin production and stress tolerance to the RpoS-mutant of Pf-5. The RpoS-mutant overproduced pyoluteorin and 2,4-diacetylphloroglucinol, two antibiotics that inhibit growth of the phytopathogenic fungus Pythium ultimum, and was superior to the wild type in suppression of seedling damping-off of cucumber caused by Pythium ultimum. When inoculated onto cucumber seed at high cell densities, the RpoS-mutant did not survive as well as the wild-type strain on surfaces of developing seedlings. Other stationary-phase-specific phenotypes of Pf-5, such as the production of cyanide and extracellular protease(s) were expressed by the RpoS-mutant, suggesting that a-s is only one of the sigma factors required for the transcription of genes in stationary-phase cells of P. fluorescens. These results indicate that a sigma factor encoded by rpoS influences antibiotic production, biological control activity, and survival of P. fluorescens on plant surfaces.

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Inhibition of Septoria tritici and other phytopathogenic fungi and bacteria by Pseudomonas fluorescens and its antibiotics

Cited by 73 publications

References 17 publications

The putative permease PhlE of Pseudomonas fluorescens F113 has a role in 2,4-diacetylphloroglucinol resistance and in general stress tolerance

The putative permease PhlE of Pseudomonas fluorescens F113 has a role in 2,4-diacetylphloroglucinol resistance and in general stress tolerance

Characterization of Interactions between the Transcriptional Repressor PhlF and Its Binding Site at the phlA Promoter in Pseudomonas fluorescens F113

The sigma factor sigma s affects antibiotic production and biological control activity of Pseudomonas fluorescens Pf-5.

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