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- Title
MexEF-OprN multidrug efflux pump transporter negatively controls N-acyl-homoserine lactone accumulation in pseudomonas syringae pv. Tabaci 6605.
- Authors
Sawada, Takahiro; Eguchi, Miho; Asaki, Seiya; Kashiwagi, Ryota; Shimomura, Kousuke; Taguchi, Fumiko; Matsui, Hidenori; Yamamoto, Mikihiro; Noutoshi, Yoshiteru; Toyoda, Kazuhiro; Ichinose, Yuki
- Abstract
Our previous studies revealed that flagellar-motility-defective mutants such as ∆fliC of Pseudomonas syringae pv. tabaci 6605 (Pta6605) have remarkably reduced production of N-acyl-homoserine lactones (AHL), quorum-sensing molecules. To investigate the reason of loss of AHL production in ∆fliC mutant, we carried out transposon mutagenesis. Among approximately 14,000 transconjugants, we found 11 AHL production-recovered (APR) strains. In these APR strains, a transposon was inserted into either mexE or mexF, genes encoding for the multidrug efflux pump transporter MexEF-OprN, and mexT, a gene encoding a putative transcriptional activator for mexEF-oprN. These results suggest that MexEF-OprN is a negative regulator of AHL production. To confirm the negative effect of MexEF-OprN on AHL production, loss- and gain-of-function experiments for mexEF-oprN were carried out. The ∆fliC∆mexF and ∆fliC∆mexT double mutant strains recovered AHL production, whereas the mexT overexpressing strain abolished AHL production, although the psyI, a gene encoding AHL synthase, is transcribed as wild type. Introduction of a mexF or mexT mutation into another flagellar-motility- and AHL production-defective mutant strain, ∆motCD, also recovered the ability to produce AHL. Furthermore, introduction of the mexF mutation into other AHL production-defective mutant strains such as ∆gacA and ∆aefR also recovered AHL production but not to the ∆psyI mutant. These results indicate that MexEF-OprN is a decisive negative determinant of AHL production and accumulation.
- Subjects
MULTIDRUG transporters; QUORUM sensing; LACTONES; PSEUDOMONAS syringae; GENETIC mutation
- Publication
Molecular Genetics & Genomics, 2018, Vol 293, Issue 4, p907
- ISSN
1617-4615
- Publication type
Article
- DOI
10.1007/s00438-018-1430-9