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Three independent signalling pathways repress motility in Pseudomonas fluorescens F113

Motility is one of the most important traits for rhizosphere colonization by pseudomonads. Despite this importance, motility is severely repressed in the rhizosphere‐colonizing strain Pseudomonas fluorescens F113. This bacterium is unable to swarm under laboratory conditions and produce relatively s...

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Autores principales: Navazo, Ana, Barahona, Emma, Redondo‐Nieto, Miguel, Martínez‐Granero, Francisco, Rivilla, Rafael, Martín, Marta
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815909/
https://www.ncbi.nlm.nih.gov/pubmed/21255280
http://dx.doi.org/10.1111/j.1751-7915.2009.00103.x
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author Navazo, Ana
Barahona, Emma
Redondo‐Nieto, Miguel
Martínez‐Granero, Francisco
Rivilla, Rafael
Martín, Marta
author_facet Navazo, Ana
Barahona, Emma
Redondo‐Nieto, Miguel
Martínez‐Granero, Francisco
Rivilla, Rafael
Martín, Marta
author_sort Navazo, Ana
collection PubMed
description Motility is one of the most important traits for rhizosphere colonization by pseudomonads. Despite this importance, motility is severely repressed in the rhizosphere‐colonizing strain Pseudomonas fluorescens F113. This bacterium is unable to swarm under laboratory conditions and produce relatively small swimming haloes. However, phenotypic variants with the ability to swarm and producing swimming haloes up to 300% larger than the wild‐type strain, arise during rhizosphere colonization. These variants harbour mutations in the genes encoding the GacA/GacS two‐component system and in other genes. In order to identify genes and pathways implicated in motility repression, we have used generalized mutagenesis with transposons. Analysis of the mutants has shown that besides the Gac system, the Wsp system and the sadB gene, which have been previously implicated in cyclic di‐GMP turnover, are implicated in motility repression: mutants in the gacS, sadB or wspR genes can swarm and produce swimming haloes larger than the wild‐type strain. Epistasis analysis has shown that the pathways defined by each of these genes are independent, because double and triple mutants show an additive phenotype. Furthermore, GacS, SadB and WspR act at different levels. Expression of the fleQ gene, encoding the master regulator of flagella synthesis is higher in the gacS(‐) and sadB(‐) backgrounds than in the wild‐type strain and this differential expression is reflected by a higher secretion of the flagellin protein FliC. Conversely, no differences in fleQ expression or FliC secretion were observed between the wild‐type strain and the wspR(‐) mutant.
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spelling pubmed-38159092014-02-12 Three independent signalling pathways repress motility in Pseudomonas fluorescens F113 Navazo, Ana Barahona, Emma Redondo‐Nieto, Miguel Martínez‐Granero, Francisco Rivilla, Rafael Martín, Marta Microb Biotechnol Special Issue: Life of microbes that interact with plants
Guest Editors: Dr. Ana Segura, Dr. Gail Preston and Professor Pierre de Wit Motility is one of the most important traits for rhizosphere colonization by pseudomonads. Despite this importance, motility is severely repressed in the rhizosphere‐colonizing strain Pseudomonas fluorescens F113. This bacterium is unable to swarm under laboratory conditions and produce relatively small swimming haloes. However, phenotypic variants with the ability to swarm and producing swimming haloes up to 300% larger than the wild‐type strain, arise during rhizosphere colonization. These variants harbour mutations in the genes encoding the GacA/GacS two‐component system and in other genes. In order to identify genes and pathways implicated in motility repression, we have used generalized mutagenesis with transposons. Analysis of the mutants has shown that besides the Gac system, the Wsp system and the sadB gene, which have been previously implicated in cyclic di‐GMP turnover, are implicated in motility repression: mutants in the gacS, sadB or wspR genes can swarm and produce swimming haloes larger than the wild‐type strain. Epistasis analysis has shown that the pathways defined by each of these genes are independent, because double and triple mutants show an additive phenotype. Furthermore, GacS, SadB and WspR act at different levels. Expression of the fleQ gene, encoding the master regulator of flagella synthesis is higher in the gacS(‐) and sadB(‐) backgrounds than in the wild‐type strain and this differential expression is reflected by a higher secretion of the flagellin protein FliC. Conversely, no differences in fleQ expression or FliC secretion were observed between the wild‐type strain and the wspR(‐) mutant. Blackwell Publishing Ltd 2009-07 2009-06-15 /pmc/articles/PMC3815909/ /pubmed/21255280 http://dx.doi.org/10.1111/j.1751-7915.2009.00103.x Text en Copyright © 2009 The Authors. Journal compilation © 2009 Society for Applied Microbiology and Blackwell Publishing Ltd
spellingShingle Special Issue: Life of microbes that interact with plants
Guest Editors: Dr. Ana Segura, Dr. Gail Preston and Professor Pierre de Wit
Navazo, Ana
Barahona, Emma
Redondo‐Nieto, Miguel
Martínez‐Granero, Francisco
Rivilla, Rafael
Martín, Marta
Three independent signalling pathways repress motility in Pseudomonas fluorescens F113
title Three independent signalling pathways repress motility in Pseudomonas fluorescens F113
title_full Three independent signalling pathways repress motility in Pseudomonas fluorescens F113
title_fullStr Three independent signalling pathways repress motility in Pseudomonas fluorescens F113
title_full_unstemmed Three independent signalling pathways repress motility in Pseudomonas fluorescens F113
title_short Three independent signalling pathways repress motility in Pseudomonas fluorescens F113
title_sort three independent signalling pathways repress motility in pseudomonas fluorescens f113
topic Special Issue: Life of microbes that interact with plants
Guest Editors: Dr. Ana Segura, Dr. Gail Preston and Professor Pierre de Wit
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815909/
https://www.ncbi.nlm.nih.gov/pubmed/21255280
http://dx.doi.org/10.1111/j.1751-7915.2009.00103.x
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