title: Mycobacterium abscessussubsp.abscessusIs Capable of DegradingPseudomonas aeruginosaQuinolone Signals.
abstract: Pseudomonas aeruginosaemploys 2-heptyl-3-hydroxy-4(1H)-quinolone (thePseudomonasquinolone signal, PQS) and 2-heptyl-4(1H)-quinolone (HHQ) as quorum sensing signal molecules, which contribute to a sophisticated regulatory network controlling the production of virulence factors and antimicrobials. We demonstrate thatMycobacterium abscessusTand clinicalM. abscessusisolates are capable of degrading these alkylquinolone signals. Genome sequences of 50 clinicalM. abscessusisolates indicated the presence ofaqdRABCgenes, contributing to fast degradation of HHQ and PQS, inM. abscessussubsp.abscessusstrains, but not inM. abscessussubsp.bolletiiandM. abscessussubsp.massilienseisolates. A subset of 18M. a. subsp.abscessusisolates contained the same five single nucleotide polymorphisms (SNPs) compared to theaqdregion of the type strain. Interestingly, representatives of these isolates showed faster PQS degradation kinetics than theM. abscessustype strain. One of the SNPs is located in the predicted promoter region of theaqdRgene encoding a putative transcriptional regulator, and two others lead to a variant of the AqdC protein termed AqdCII, which differs in two amino acids from AqdCIof the type strain. AqdC, the key enzyme of the degradation pathway, is a PQS dioxygenase catalyzing quinolone ring cleavage. While transcription ofaqdRandaqdCis induced by PQS, transcript levels in a representative of the subset of 18 isolates were not significantly altered despite the detected SNP in the promoter region. However, purified recombinant AqdCIIand AqdCIexhibit different kinetic properties, with approximate apparentKmvalues for PQS of 14 μM and 37 μM, andkcatvalues of 61 s-1and 98 s-1, respectively, which may (at least in part) account for the observed differences in PQS degradation rates of the strains. In co-culture experiments ofP. aeruginosaPAO1 andM. abscessus, strains harboring theaqdgenes reduced the PQS levels, whereas mycobacteria lacking theaqdgene cluster even boosted PQS production. The results suggest that the presence and expression of theaqdgenes inM. abscessuslead to a competitive advantage againstP. aeruginosa.
authors.affiliation: Institute for Molecular Microbiology and Biotechnology, University of Münster Münster, Germany.
authors.forename: Franziska S
authors.initials: FS
authors.lastname: Birmes
authors.affiliation: Center for Biotechnology (CeBiTec) Bielefeld, Germany.
authors.forename: Timo
authors.initials: T
authors.lastname: Wolf
authors.affiliation: Research Center BorstelSülfeld, Germany; German Center for Infection ResearchBorstel, Germany.
authors.forename: Thomas A
authors.initials: TA
authors.lastname: Kohl
authors.affiliation: Institute for Medical Microbiology and Hospital Epidemiology, Hannover Medical School Hannover, Germany.
authors.forename: Kai
authors.initials: K
authors.lastname: Rüger
authors.affiliation: Institute for Medical Microbiology and Hospital Epidemiology, Hannover Medical School Hannover, Germany.
authors.forename: Franz
authors.initials: F
authors.lastname: Bange
authors.affiliation: Center for Biotechnology (CeBiTec) Bielefeld, Germany.
authors.forename: Jörn
authors.initials: J
authors.lastname: Kalinowski
authors.affiliation: Institute for Molecular Microbiology and Biotechnology, University of Münster Münster, Germany.
authors.forename: Susanne
authors.initials: S
authors.lastname: Fetzner
keywords: Mycobacterium abscessus; Pseudomonas aeruginosa; Pseudomonas quinolone signal; alkylquinolone degradation; quorum quenching; quorum sensing