Structural analyses of the AAA+ ATPase domain of the transcriptional regulator GtrR in the BDSF quorum sensing system in Burkholderia cenocepacia

FEBS Letters ◽  
2021 ◽  
Author(s):  
Xin‐Fu Yan ◽  
Chunxi Yang ◽  
Mingfang Wang ◽  
Yonlada Yong ◽  
Yinyue Deng ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Transcriptional Regulator ◽  
Burkholderia Cenocepacia ◽  
Atpase Domain ◽  
Aaa Atpase ◽  
Sensing System ◽  
Quorum Sensing System

The CepIR quorum-sensing system contributes to the virulence of Burkholderia cenocepacia respiratory infections

Microbiology ◽  
2003 ◽  
Vol 149 (12) ◽  
pp. 3649-3658 ◽  
Author(s):  
P. A. Sokol ◽  
U. Sajjan ◽  
M. B. Visser ◽  
S. Gingues ◽  
J. Forstner ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Parent Strain ◽  
Respiratory Infections ◽  
Virulent Strain ◽  
Interleukin 1 ◽  
Homoserine Lactone ◽  
Burkholderia Cenocepacia ◽  
Sensing System ◽  
Quorum Sensing System ◽  
The Difference

The cepIR genes encode an N-acyl homoserine lactone (AHL)-dependent quorum-sensing system consisting of an AHL synthase that directs the synthesis of N-octanoyl-l-homoserine lactone (ohl) and n-hexanoyl-l-homoserine lactone and a transcriptional regulator. The virulence of cepIR mutants was examined in two animal models. Rats were infected with agar beads containing Burkholderia cenocepacia K56-2, K56-I2 (cepI : : Tpr) or K56-R2 (cepR : : Tn5-OT182). At 10 days post-infection, the extent of lung histopathological changes was significantly lower in lungs infected with K56-I2 or K56-R2 compared to the parent strain. Intranasal infections were performed in Cftr (−/−) mice and their wild-type siblings. K56-2 was more virulent in both groups of mice. K56-I2 was the least virulent strain and was not invasive in the Cftr (−/−) mice. OHL was readily detected in lung homogenates from Cftr (−/−) mice infected with K56-2 but was only detected at levels slightly above background in a few mice infected with K56-I2. Lung homogenates from mice infected with K56-2 had significantly higher levels of the inflammatory mediators murine macrophage inflammatory protein-2, KC/N51, interleukin-1β and interleukin-6 than those from K56-I2-infected animals. These studies indicate that a functional CepIR quorum-sensing system contributes to the severity of B. cenocepacia infections. A zinc metalloprotease gene (zmpA) was shown to be regulated by CepR and may be one of the factors that accounts for the difference in virulence between the cepI mutant and the parent strain.

scholarly journals Functions Required for Extracellular Quinolone Signaling by Pseudomonas aeruginosa

2002 ◽  
Vol 184 (23) ◽  
pp. 6472-6480 ◽  
Author(s):  
Larry A. Gallagher ◽  
Susan L. McKnight ◽  
Marina S. Kuznetsova ◽  
Everett C. Pesci ◽  
Colin Manoil
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Secondary Metabolites ◽  
Regulatory Network ◽  
Biosynthetic Pathway ◽  
Extracellular Enzymes ◽  
Transcriptional Regulator ◽  
Transposon Mutagenesis ◽  
Sensing System ◽  
Quorum Sensing System

ABSTRACT A set of 30 mutants exhibiting reduced production of the phenazine poison pyocyanin were isolated following transposon mutagenesis of Pseudomonas aeruginosa PAO1. The mutants could be subdivided into those with defects in the primary phenazine biosynthetic pathway and those with more pleiotropic defects. The largest set of pleiotropic mutations blocked the production of the extracellular Pseudomonas quinolone signal (PQS), a molecule required for the synthesis of secondary metabolites and extracellular enzymes. Most of these pqs mutations affected genes which appear to encode PQS biosynthetic functions, although a transcriptional regulator and an apparent response effector were also represented. Two of the genes required for PQS synthesis (phnA and phnB) had previously been assumed to encode phenazine biosynthetic functions. The transcription of one of the genes required for PQS synthesis (PA2587/pqsH) was regulated by the LasI/R quorum-sensing system, thereby linking quorum sensing and PQS regulation. Others of the pleiotropic phenazine-minus mutations appear to inactivate novel components of the quorum-sensing regulatory network, including one regulator (np20) previously shown to be required for virulence in neutropenic mice.

scholarly journals Loci identification of a N-acyl homoserine lactone type quorum sensing system and a new LysR-type transcriptional regulator associated with antimicrobial activity and swarming in Burkholderia gladioli UAPS07070

2019 ◽  
Vol 14 (1) ◽  
pp. 165-178
Author(s):  
E. Seynos-García ◽  
M. Castañeda-Lucio ◽  
J. Muñoz-Rojas ◽  
L. López-Pliego ◽  
M. Villalobos ◽  
...  
Keyword(s):  
Antimicrobial Activity ◽  
Quorum Sensing ◽  
Transcriptional Regulator ◽  
Homoserine Lactone ◽  
Sensing System ◽  
Gene Coding ◽  
Burkholderia Gladioli ◽  
Quorum Sensing System ◽  
First Time ◽  
Random Transposition

AbstractA random transposition mutant library of B. gladioli UAPS07070 was analyzed for searching mutants with impaired microbial antagonism. Three derivates showed diminished antimicrobial activity against a sensitive strain. The mutated loci showed high similarity to the quorum sensing genes of the AHL-synthase and its regulator. Another mutant was affected in a gene coding for a LysrR-type transcriptional regulator. The production of toxoflavin, the most well known antimicrobial-molecule and a major virulence factor of plant-pathogenic B. glumae and B. gladioli was explored. The absence of a yellowish pigment related to toxoflavin and the undetectable transcription of toxA in the mutants indicated the participation of the QS system and of the LysR-type transcriptional regulator in the regulation of toxoflavin. Additionally, those genes were found to be related to the swarming phenotype. Lettuce inoculated with the AHL synthase and the lysR mutants showed less severe symptoms. We present evidence of the participation of both, the quorum sensing and for the first time, of a LysR-type transcriptional regulator in antibiosis and swarming phenotype in a strain of B. gladioli

scholarly journals Identification of Genes Regulated by the cepIR Quorum-Sensing System in Burkholderia cenocepacia by High-Throughput Screening of a Random Promoter Library

2006 ◽  
Vol 189 (3) ◽  
pp. 968-979 ◽  
Author(s):  
Benchamas Subsin ◽  
Catherine E. Chambers ◽  
Michelle B. Visser ◽  
Pamela A. Sokol
Keyword(s):  
Quorum Sensing ◽  
Expression Profiles ◽  
Burkholderia Cenocepacia ◽  
Mrna Levels ◽  
Gene Promoters ◽  
Wild Type ◽  
Sensing System ◽  
Promoter Library ◽  
A Genome ◽  
Quorum Sensing System

ABSTRACT The Burkholderia cenocepacia cepIR quorum-sensing system regulates expression of extracellular proteases, chitinase, and genes involved in ornibactin biosynthesis, biofilm formation, and motility. In a genome-wide screen we identified cepIR-regulated genes by screening a random promoter library of B. cenocepacia K56-2 constructed in a luminescence reporter detection plasmid for differential expression in response to N-octanoyl-l-homoserine lactone (OHL). Eighty-nine clones were identified; in 58 of these clones expression was positively regulated by cepIR, and in 31 expression was negatively regulated by cepIR. The expression profiles of the 89 promoter clones were compared in the cepI mutant K56-dI2 in medium supplemented with 30 pM OHL and K56-2 to confirm that the presence of OHL restored expression to wild-type levels. To validate the promoter library observations and to determine the effect of a cepR mutation on expression of selected genes, the mRNA levels of nine genes whose promoters were predicted to be regulated by cepR were quantitated by quantitative reverse transcription-PCR in the wild type and cepI and cepR mutants. The expression levels of all nine genes were similar in the cepI and cepR mutants and consistent with the promoter-lux reporter activity. The expression of four selected cepIR-regulated gene promoters was examined in a cciIR mutant, and two of these promoters were also regulated by cciIR. This study extends our understanding of genes whose expression is influenced by cepIR and indicates the global regulatory effect of the cepIR system in B. cenocepacia.

scholarly journals Quorum-Sensing Regulation of a Copper Toxicity System in Pseudomonas aeruginosa

2010 ◽  
Vol 192 (10) ◽  
pp. 2557-2568 ◽  
Author(s):  
Joshua T. Thaden ◽  
Stephen Lory ◽  
Timothy S. Gardner
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Molecular Genetic ◽  
Copper Toxicity ◽  
Transcriptional Regulator ◽  
Global Gene Expression ◽  
Copper Resistance ◽  
Binding Motif ◽  
Sensing System ◽  
Quorum Sensing System

ABSTRACT The LasR/LasI quorum-sensing system in Pseudomonas aeruginosa influences global gene expression and mediates pathogenesis. In this study, we show that the quorum-sensing system activates, via the transcriptional regulator PA4778, a copper resistance system composed of 11 genes. The quorum-sensing global regulator LasR was recently shown to directly activate transcription of PA4778, a cueR homolog and a MerR-type transcriptional regulator. Using molecular genetic methods and bioinformatics, we verify the interaction of LasR with the PA4778 promoter and further demonstrate the LasR binding site. We also identify a putative PA4778 binding motif and show that the protein directly binds to and activates five promoters controlling the expression of 11 genes—PA3519 to -15, PA3520, mexPQ-opmE, PA3574.1, and cueA, a virulence factor in a murine model. Using gene disruptions, we show that PA4778, along with 7 of 11 gene targets of PA4778, increases the sensitivity of P. aeruginosa to elevated copper concentrations. This work identifies a cellular function for PA4778 and four other previously unannotated genes (PA3515, PA3516, PA3517, and PA3518) and suggests a potential role for copper in the quorum response. We propose to name PA4778 cueR.

scholarly journals Characterization of the cciIR Quorum-Sensing System in Burkholderia cenocepacia

2005 ◽  
Vol 73 (8) ◽  
pp. 4982-4992 ◽  
Author(s):  
Rebecca J. Malott ◽  
Adam Baldwin ◽  
Eshwar Mahenthiralingam ◽  
Pamela A. Sokol
Keyword(s):  
Quorum Sensing ◽  
Protease Activity ◽  
Parent Strain ◽  
Response Regulator ◽  
Homoserine Lactone ◽  
Burkholderia Cenocepacia ◽  
Pcr Analysis ◽  
Swarming Motility ◽  
Sensing System ◽  
Quorum Sensing System

ABSTRACT Several transmissible Burkholderia cenocepacia strains that infect multiple cystic fibrosis patients contain a genomic island designated as the cenocepacia island (cci). The cci contains a predicted N-acylhomoserine lactone (AHL) synthase gene, cciI, and a predicted response regulator gene, cciR. AHL production profiles indicated that CciI catalyzes the synthesis of N-hexanoyl-l-homoserine lactone and minor amounts of N-octanoyl-l-homoserine lactone. The cciI and cciR genes were found to be cotranscribed by reverse transcription-PCR analysis, and the expression of a cciIR::luxCDABE fusion in a cciR mutant suggested that the cciIR system negatively regulates its own expression. B. cenocepacia strains also have a cepIR quorum-sensing system. Expression of cepI::luxCDABE or cepR::luxCDABE fusions in a cciR mutant showed that CciR negatively regulates cepI but does not regulate cepR. Expression of the cciIR::luxCDABE fusion in a cepR mutant indicated that functional CepR is required for cciIR expression. Phylogenetic analysis suggested that the cciIR system was acquired by horizontal gene transfer from a distantly related organism and subsequently incorporated into the ancestral cepIR regulatory network. Mutations in cciI, cciR, cepI cciI, and cepR cciR were constructed in B. cenocepacia K56-2. The cciI mutant had greater protease activity and less swarming motility than the parent strain. The cciR mutant had less protease activity than the parent strain. The phenotypes of the cepI cciI and cepR cciR mutants were similar to cepI or cepR mutants, with less protease activity and swarming motility than the parent strain.

Sign in / Sign up

Export Citation Format

Share Document