Complete genome sequence of Rhodococcus erythropolis BG43 (DSM 46869), a degrader of Pseudomonas aeruginosa quorum sensing signal molecules

Rückert, Christian; Birmes, Franziska S.; Müller, Christine; Niewerth, Heiko; Winkler, Anderson M.; Fetzner, Susanne; Kalinowski, Jörn

doi:10.1016/j.jbiotec.2015.07.014

Cited by 7 publications

(11 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Recently, we isolated Rhodococcus erythropolis strain BG43, which is capable of degrading HHQ and PQS to anthranilic acid (37,38). In the present study, we identified two sets of PQS-inducible genes located on a plasmid of strain BG43, which code for the enzymes of the degradation pathway.…”

mentioning

confidence: 84%

Rhodococcus erythropolis BG43 Genes Mediating Pseudomonas aeruginosa Quinolone Signal Degradation and Virulence Factor Attenuation

Müller

Birmes

Rückert

et al. 2015

Appl Environ Microbiol

Self Cite

View full text Add to dashboard Cite

bRhodococcus erythropolis BG43 is able to degrade the Pseudomonas aeruginosa quorum sensing signal molecules PQS (Pseudomonas quinolone signal) [2-heptyl-3-hydroxy-4(1H)-quinolone] and HHQ [2-heptyl-4(1H)-quinolone] to anthranilic acid. Based on the hypothesis that degradation of HHQ might involve hydroxylation to PQS followed by dioxygenolytic cleavage of the heterocyclic ring and hydrolysis of the resulting N-octanoylanthranilate, the genome was searched for corresponding candidate genes. Two gene clusters, aqdA1B1C1 and aqdA2B2C2, each predicted to code for a hydrolase, a flavin monooxygenase, and a dioxygenase related to 1H-3-hydroxy-4-oxoquinaldine 2,4-dioxygenase, were identified on circular plasmid pRLCBG43 of strain BG43. Transcription of all genes was upregulated by PQS, suggesting that both gene clusters code for alkylquinolone-specific catabolic enzymes. An aqdR gene encoding a putative transcriptional regulator, which was also inducible by PQS, is located adjacent to the aqdA2B2C2 cluster. Expression of aqdA2B2C2 in Escherichia coli conferred the ability to degrade HHQ and PQS to anthranilic acid; however, for E. coli transformed with aqdA1B1C1, only PQS degradation was observed. Purification of the recombinant AqdC1 protein verified that it catalyzes the cleavage of PQS to form N-octanoylanthranilic acid and carbon monoxide and revealed apparent K m and k cat values for PQS of ϳ27 M and 21 s ؊1 , respectively. Heterologous expression of the PQS dioxygenase gene aqdC1 or aqdC2 in P. aeruginosa PAO1 quenched the production of the virulence factors pyocyanin and rhamnolipid and reduced the synthesis of the siderophore pyoverdine. Thus, the toolbox of quorum-quenching enzymes is expanded by new PQS dioxygenases.A wide variety of bacteria employ quorum sensing (QS) systems to communicate and coordinate their behavior according to their cell density by sensing self-generated small signal molecules (1). QS systems allow bacteria to act cooperatively in processes such as biofilm formation or pathogenesis. The opportunistic pathogen Pseudomonas aeruginosa uses a complex QS network comprising several interconnected signaling circuits to regulate group motility, biofilm maturation, and a battery of virulence factors (for a recent review, see reference 2). The Las and Rhl circuits use the signal molecules N-3-oxo-dodecanoyl homoserine lactone (3OC12-HSL) and N-butanoyl homoserine lactone (C4-HSL), respectively, whereas the Pqs circuit employs the alkylquinolone (AQ) signals 2-heptyl-3-hydroxy-4(1H)-quinolone (Pseudomonas quinolone signal [PQS]) and 2-heptyl-4(1H)-quinolone (HHQ), which act as coinducers of the transcriptional regulator PqsR (3-6). The PqsR-AQ complex mainly activates the transcription of the pqsABCDE operon coding for the enzymes of AQ biosynthesis (7, 8); moreover, PqsE, via unknown mechanisms, modulates the expression of large arrays of target genes (9-11). PqsE was termed the "PQS response protein," because its disruption negatively affected the production of PQS-mediated exoproducts (3,9,12...

show abstract

mentioning

confidence: 84%

Rhodococcus erythropolis BG43 Genes Mediating Pseudomonas aeruginosa Quinolone Signal Degradation and Virulence Factor Attenuation

Müller

Birmes

Rückert

et al. 2015

Appl Environ Microbiol

Self Cite

View full text Add to dashboard Cite

show abstract

“…Among these contigs, 12 did not match the circular PacBio assembly, which showed the highest similarities to plasmid sequences of other R. erythropolis strains (17). To confirm the possibility that these contigs were derived from plasmid sequences, we examined their connectivity by PCR and finally obtained another 85-kb circular sequence and a 241-kb linear sequence.…”

Section: Announcementmentioning

confidence: 99%

Genome Sequence of Rhodococcus erythropolis Type Strain JCM 3201

Yoshida

Kitagawa

Ishiya

et al. 2019

Microbiol Resour Announc

View full text Add to dashboard Cite

show abstract

“…In this context, attention has been focused on strategies for interfering with the quorum sensing (QS) systems of pathogenic bacteria, in order to target their pathogenicity/virulence and to develop new anti-infective therapies. QS is an intercellular communication system mediated by diffusible chemical signal molecules termed autoinducers (AIs) that control gene expression patterns and therefore allows bacteria to synchronize their behavior [ 8 ]. In many cases, the responses prompted by QS signals contribute directly to pathogenesis through the production of virulence determinants, such as toxins and proteases.…”

Section: Introductionmentioning

confidence: 99%

Cobalt Complex with Thiazole-Based Ligand as New Pseudomonas aeruginosa Quorum Quencher, Biofilm Inhibitor and Virulence Attenuator

et al. 2018

View full text Add to dashboard Cite

Pseudomonas aeruginosa is one of the most dreaded human pathogens, because of its intrinsic resistance to a number of commonly used antibiotics and ability to form sessile communities (biofilms). Innovative treatment strategies are required and that can rely on the attenuation of the pathogenicity and virulence traits. The interruption of the mechanisms of intercellular communication in bacteria (quorum sensing) is one of such promising strategies. A cobalt coordination compound (Co(HL)2) synthesized from (E)-2-(2-(pyridin-2-ylmethylene)hydrazinyl)-4-(p-tolyl)thiazole (HL) is reported herein for the first time to inhibit P. aeruginosa 3-oxo-C12-HSL-dependent QS system (LasI/LasR system) and underling phenotypes (biofilm formation and virulence factors). Its interactions with a possible target, the transcriptional activator protein complex LasR-3-oxo-C12-HSL, was studied by molecular modeling with the coordination compound ligand having stronger predicted interactions than those of co-crystallized ligand 3-oxo-C12-HSL, as well as known-binder furvina. Transition metal group 9 coordination compounds may be explored in antipathogenic/antibacterial drug design.

show abstract

Complete genome sequence of Rhodococcus erythropolis BG43 (DSM 46869), a degrader of Pseudomonas aeruginosa quorum sensing signal molecules

Cited by 7 publications

References 11 publications

Rhodococcus erythropolis BG43 Genes Mediating Pseudomonas aeruginosa Quinolone Signal Degradation and Virulence Factor Attenuation

Rhodococcus erythropolis BG43 Genes Mediating Pseudomonas aeruginosa Quinolone Signal Degradation and Virulence Factor Attenuation

Genome Sequence of Rhodococcus erythropolis Type Strain JCM 3201

Cobalt Complex with Thiazole-Based Ligand as New Pseudomonas aeruginosa Quorum Quencher, Biofilm Inhibitor and Virulence Attenuator

Contact Info

Product

Resources

About