title: Pseudomonas fluorescens F113 mutant with enhanced competitive colonization ability and improved biocontrol activity against fungal root pathogens.
abstract: Motility is one of the most important traits for efficient rhizosphere colonization by Pseudomonas fluorescens F113rif (F113). In this bacterium, motility is a polygenic trait that is repressed by at least three independent pathways, including the Gac posttranscriptional system, the Wsp chemotaxis-like pathway, and the SadB pathway. Here we show that the kinB gene, which encodes a signal transduction protein that together with AlgB has been implicated in alginate production, participates in swimming motility repression through the Gac pathway, acting downstream of the GacAS two-component system. Gac mutants are impaired in secondary metabolite production and are unsuitable as biocontrol agents. However, the kinB mutant and a triple mutant affected in kinB, sadB, and wspR (KSW) possess a wild-type phenotype for secondary metabolism. The KSW strain is hypermotile and more competitive for rhizosphere colonization than the wild-type strain. We have compared the biocontrol activity of KSW with those of the wild-type strain and a phenotypic variant (F113v35 [V35]) which is hypermotile and hypercompetitive but is affected in secondary metabolism since it harbors a gacS mutation. Biocontrol experiments in the Fusarium oxysporum f. sp. radicis-lycopersici/Lycopersicum esculentum (tomato) and Phytophthora cactorum/Fragaria vesca (strawberry) pathosystems have shown that the three strains possess biocontrol activity. Biocontrol activity was consistently lower for V35, indicating that the production of secondary metabolites was the most important trait for biocontrol. Strain KSW showed improved biocontrol compared with the wild-type strain, indicating that an increase in competitive colonization ability resulted in improved biocontrol and that the rational design of biocontrol agents by mutation is feasible.
authors.affiliation: Departamento de Biología, Universidad Autónoma de Madrid, 28049 Madrid, Spain.
authors.forename: Emma
authors.initials: E
authors.lastname: Barahona
authors.forename: Ana
authors.initials: A
authors.lastname: Navazo
authors.forename: Francisco
authors.initials: F
authors.lastname: Martínez-Granero
authors.forename: Teresa
authors.initials: T
authors.lastname: Zea-Bonilla
authors.forename: Rosa María
authors.initials: RM
authors.lastname: Pérez-Jiménez
authors.forename: Marta
authors.initials: M
authors.lastname: Martín
authors.forename: Rafael
authors.initials: R
authors.lastname: Rivilla
mesh_terms: D000898:Antibiosis / Q000235:genetics / Q000502:physiology*; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D002633:Chemotaxis / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D031985:Fragaria / Q000254:growth & development*; D005670:Fusarium / Q000254:growth & development*; D015964:Gene Expression Regulation, Bacterial; D018551:Solanum lycopersicum / Q000382:microbiology; D009154:Mutation; D010572:Pest Control, Biological; D010838:Phytophthora / Q000382:microbiology; D010935:Plant Diseases / Q000235:genetics / Q000382:microbiology; D018517:Plant Roots / Q000382:microbiology*; D011551:Pseudomonas fluorescens / Q000166:cytology / Q000235:genetics / Q000378:metabolism*; D058441:Rhizosphere; D015398:Signal Transduction / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism
chemical_list: D001426:Bacterial Proteins; D004268:DNA-Binding Proteins; C091100:GacA protein, Bacteria; D014157:Transcription Factors; C072862:AlgB protein, Pseudomonas