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The Pseudomonas putida CsrA/RsmA homologues negatively affect c‐di‐GMP pools and biofilm formation through the GGDEF/EAL response regulator CfcR

Expression of cfcR, encoding the only GGDEF/EAL response regulator in Pseudomonas putida, is transcriptionally regulated by RpoS, ANR and FleQ, and the functionality of CfcR as a diguanylate cyclase requires the multisensor CHASE3/GAF hybrid histidine kinase named CfcA. Here an additional level of c...

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Autores principales: Huertas‐Rosales, Óscar, Romero, Manuel, Heeb, Stephan, Espinosa‐Urgel, Manuel, Cámara, Miguel, Ramos‐González, María Isabel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6849547/
https://www.ncbi.nlm.nih.gov/pubmed/28677348
http://dx.doi.org/10.1111/1462-2920.13848
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author Huertas‐Rosales, Óscar
Romero, Manuel
Heeb, Stephan
Espinosa‐Urgel, Manuel
Cámara, Miguel
Ramos‐González, María Isabel
author_facet Huertas‐Rosales, Óscar
Romero, Manuel
Heeb, Stephan
Espinosa‐Urgel, Manuel
Cámara, Miguel
Ramos‐González, María Isabel
author_sort Huertas‐Rosales, Óscar
collection PubMed
description Expression of cfcR, encoding the only GGDEF/EAL response regulator in Pseudomonas putida, is transcriptionally regulated by RpoS, ANR and FleQ, and the functionality of CfcR as a diguanylate cyclase requires the multisensor CHASE3/GAF hybrid histidine kinase named CfcA. Here an additional level of cfcR control, operating post‐transcriptionally via the RNA‐binding proteins RsmA, RsmE and RsmI, is unraveled. Specific binding of the three proteins to an Rsm‐binding motif (5′CANGGANG3′) encompassing the translational start codon of cfcR was confirmed. Although RsmA exhibited the highest binding affinity to the cfcR transcript, single deletions of rsmA, rsmE or rsmI caused minor derepression in CfcR translation compared to a ΔrsmIEA triple mutant. RsmA also showed a negative impact on c‐di‐GMP levels in a double mutant ΔrsmIE through the control of cfcR, which is responsible for most of the free c‐di‐GMP during stationary phase in static conditions. In addition, a CfcR‐dependent c‐di‐GMP boost was observed during this stage in ΔrsmIEA confirming the negative effect of Rsm proteins on CfcR translation and explaining the increased biofilm formation in this mutant compared to the wild type. Overall, these results suggest that CfcR is a key player in biofilm formation regulation by the Rsm proteins in P. putida.
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spelling pubmed-68495472019-11-15 The Pseudomonas putida CsrA/RsmA homologues negatively affect c‐di‐GMP pools and biofilm formation through the GGDEF/EAL response regulator CfcR Huertas‐Rosales, Óscar Romero, Manuel Heeb, Stephan Espinosa‐Urgel, Manuel Cámara, Miguel Ramos‐González, María Isabel Environ Microbiol Research Articles Expression of cfcR, encoding the only GGDEF/EAL response regulator in Pseudomonas putida, is transcriptionally regulated by RpoS, ANR and FleQ, and the functionality of CfcR as a diguanylate cyclase requires the multisensor CHASE3/GAF hybrid histidine kinase named CfcA. Here an additional level of cfcR control, operating post‐transcriptionally via the RNA‐binding proteins RsmA, RsmE and RsmI, is unraveled. Specific binding of the three proteins to an Rsm‐binding motif (5′CANGGANG3′) encompassing the translational start codon of cfcR was confirmed. Although RsmA exhibited the highest binding affinity to the cfcR transcript, single deletions of rsmA, rsmE or rsmI caused minor derepression in CfcR translation compared to a ΔrsmIEA triple mutant. RsmA also showed a negative impact on c‐di‐GMP levels in a double mutant ΔrsmIE through the control of cfcR, which is responsible for most of the free c‐di‐GMP during stationary phase in static conditions. In addition, a CfcR‐dependent c‐di‐GMP boost was observed during this stage in ΔrsmIEA confirming the negative effect of Rsm proteins on CfcR translation and explaining the increased biofilm formation in this mutant compared to the wild type. Overall, these results suggest that CfcR is a key player in biofilm formation regulation by the Rsm proteins in P. putida. John Wiley and Sons Inc. 2017-07-21 2017-09 /pmc/articles/PMC6849547/ /pubmed/28677348 http://dx.doi.org/10.1111/1462-2920.13848 Text en © 2017 The Authors. Environmental Microbiology published by Society for Applied Microbiology and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Huertas‐Rosales, Óscar
Romero, Manuel
Heeb, Stephan
Espinosa‐Urgel, Manuel
Cámara, Miguel
Ramos‐González, María Isabel
The Pseudomonas putida CsrA/RsmA homologues negatively affect c‐di‐GMP pools and biofilm formation through the GGDEF/EAL response regulator CfcR
title The Pseudomonas putida CsrA/RsmA homologues negatively affect c‐di‐GMP pools and biofilm formation through the GGDEF/EAL response regulator CfcR
title_full The Pseudomonas putida CsrA/RsmA homologues negatively affect c‐di‐GMP pools and biofilm formation through the GGDEF/EAL response regulator CfcR
title_fullStr The Pseudomonas putida CsrA/RsmA homologues negatively affect c‐di‐GMP pools and biofilm formation through the GGDEF/EAL response regulator CfcR
title_full_unstemmed The Pseudomonas putida CsrA/RsmA homologues negatively affect c‐di‐GMP pools and biofilm formation through the GGDEF/EAL response regulator CfcR
title_short The Pseudomonas putida CsrA/RsmA homologues negatively affect c‐di‐GMP pools and biofilm formation through the GGDEF/EAL response regulator CfcR
title_sort pseudomonas putida csra/rsma homologues negatively affect c‐di‐gmp pools and biofilm formation through the ggdef/eal response regulator cfcr
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6849547/
https://www.ncbi.nlm.nih.gov/pubmed/28677348
http://dx.doi.org/10.1111/1462-2920.13848
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