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A Pseudomonas fluorescens type 6 secretion system is related to mucoidy, motility and bacterial competition
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  • 作者:Victorien Decoin (1)
    Mathias Gallique (1)
    Corinne Barbey (1)
    Francois Le Mauff (2)
    Cecile Duclairoir Poc (1)
    Marc GJ Feuilloley (1)
    Nicole Orange (1)
    Annabelle Merieau (1)

    1. LMSM
    ; Laboratoire de Microbiologie Signaux et Microenvironnement ; Normandie Universit茅 ; EA 4312 ; IRIB ; Universit茅 de Rouen ; IUT d鈥橢vreux ; 55 rue Saint Germain ; 27000 ; Evreux ; France
    2. GlycoMEV
    ; Laboratoire de Glycobiologie et Matrice Extracellulaire V茅g茅tale ; Normandie Universit茅 ; EA 4358 ; Universit茅 de Rouen ; Facult茅 des sciences ; Batiment 20 Gadeau de Kerville ; IRIB 76820 ; Mont Saint-Aignan ; France
  • 关键词:Pseudomonas fluorescens ; Type 6 secretion system ; Hcp protein ; Competitive inhibition ; Motility ; Mucoidy ; Exopolysaccharides
  • 刊名:BMC Microbiology
  • 出版年:2015
  • 出版时间:December 2015
  • 年:2015
  • 卷:15
  • 期:1
  • 全文大小:2,117 KB
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  • 刊物主题:Microbiology; Biological Microscopy; Fungus Genetics; Parasitology; Virology; Life Sciences, general;
  • 出版者:BioMed Central
  • ISSN:1471-2180
文摘
Background Pseudomonas fluorescens strain MFE01 secretes in abundance two Hcp proteins (haemolysin co-regulated proteins) Hcp1 and Hcp2, characteristic of a functional type 6 secretion system. Phenotypic studies have shown that MFE01 has antibacterial activity against a wide range of competitor bacteria, including rhizobacteria and clinically relevant bacteria. Mutagenesis of the hcp2 gene abolishes or reduces, depending on the target strain, MFE01 antibacterial activity. Hcp1, encoded by hcp1, may also be involved in bacterial competition. We therefore assessed the contribution of Hcp1 to competition of P. fluorescens MFE01 with other bacteria, by studying MFE01 mutants in various competitive conditions. Results Mutation of hcp1 had pleiotropic effects on the MFE01 phenotype. It affected mucoidy of the strain and its motility and was associated with the loss of flagella, which were restored by introduction of plasmid expressing hcp1. The hcp1 mutation had no effect on bacterial competition during incubation in solid medium. MFE01 was able to sequester another P. fluorescens strain, MFN1032, under swimming conditions. The hcp2 mutant but not the hcp1 mutant conserved this ability. In competition assays on swarming medium, MFE01 impaired MFN1032 swarming and displayed killing activity. The hcp2 mutant, but not the hcp1 mutant, was able to reduce MFN1032 swarming. The hcp1 and hcp2 mutations each abolished killing activity in these conditions. Conclusion Our findings implicate type 6 secretion of Hcp1 in mucoidy and motility of MFE01. Our study is the first to establish a link between a type 6 secretion system and flagellin and mucoidy. Hcp1 also appears to contribute to limiting the motility of prey cells to facilitate killing mediated by Hcp2. Inhibition of motility associated with an Hcp protein has never been described. With this work, we illustrate the importance and versatility of type 6 secretion systems in bacterial adaptation and fitness.

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