Unravelling the genome-wide contributions of specific 2-alkyl-4-quinolones and PqsE to quorum sensing in Pseudomonas aeruginosa

ABSTRACT: Pseudomonas aeruginosa pathogenicity mainly relies on its ability to finely control the expression of virulence determinants via multiple quorum sensing (QS) systems. Despite the relevant role of the pqs QS system in controlling the expression of key virulence factors and biofilm formation in P. aeruginosa, our understanding of the molecular mechanisms governing this QS circuit, which employs 2-alkyl-4-quinolones (AQs) as signal molecules, is still preliminary, probably due to its complexity. Multiple genes are required for the synthesis of the primary AQs, 2-heptyl-4-hydroxyquinoline (HHQ), 2-heptyl-3-hydroxy-4-quinolone (PQS), and 2-heptyl-4-hydroxyquinoline N-oxide (HQNO). These include the pqsABCDE operon, required for the synthesis of HHQ, which in turn is oxidized to PQS via the action of the monooxygenase PqsH. The monooxygenase PqsL is required for HQNO synthesis together with the pqsABCD genes. The fifth gene of the pqsABCDE operon, pqsE, is also required for the production of major virulence factors and for biofilm formation, and exerts a homeostatic effect on AQs synthesis by repressing the transcription of the pqsABCDE operon. The pqs system is subject to positive autoregulation, with the PqsR regulator promoting pqsABCDE transcription upon binding to HHQ or PQS. However, the individual contributions and relative importance of HHQ, PQS, HQNO and PqsE to AQ-dependent signalling is not fully apparent, because of the overlapping and interdependent nature of the factors involved in this complex QS network. We used microarrays to detail the global response of a P. aeruginosa mutant strain unable to synthesise or convert AQs, and to express PqsE to exogenously provided AQs or IPTG (to induce pqsE expression).

ORGANISM(S): Pseudomonas aeruginosa Pseudomonas aeruginosa PAO1

PROVIDER: GSE81364 | GEO | 2020/11/21

REPOSITORIES: GEO