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Category: Microbial Genetics and Molecular Biology; Bacterial Pathogenesis
Quorum Sensing in the Soft-Rot Erwinias, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555815578/9781555814045_Chap12-1.gif /docserver/preview/fulltext/10.1128/9781555815578/9781555814045_Chap12-2.gifAbstract:
One of the first bacterial species for which N-acylhomoserine lactone (AHL) quorum sensing (QS) was described was Erwinia carotovora. Since then, QS has been well studied in the soft-rot erwinias, where, as described in this chapter, QS plays a key role in the regulation of secreted plant cell wall-degrading enzymes (PCWDEs) production and hence in virulence. In certain strains, a well-defined AHL QS system also controls production of β-lactam antibiotic, carbapenem. In addition, it must be emphasized that QS is only one of many regulatory inputs into virulence factor production in Erwinia. The majority of the key secreted virulence factors of E. carotovora and E. chrysanthemi, including multiple Pels, Peh, Cel, and Svx, are secreted by a type II secretion system known as the Out system. There have been two reports describing the existence of AHL QS in E. amylovora. First, production of a single AHL, most likely 3-oxo-C6-HSL, was described for several Italian strains of E. amylovora; for one strain, production of AHL was observed in planta. Second, AHL activity was detected in the culture supernatant of a Swiss strain of E. amylovora. Both reports describe the detection and partial sequencing of pairs of convergent luxIR homologues, named eamIR.
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Regulation of carbapenem antibiotic (Car) production by AHL QS in E. carotovora subsp. carotovora ATCC 39048. The signaling molecule, 3-oxo-C6-HSL, is synthesized by CarI. At low cell densities (top), 3-oxo-C6-HSL diffuses away from the cell and CarR is in a transcriptionally inactive state. The carA-H gene cluster is not transcribed from the QS-dependent promoter (PQS) upstream of carA; hence, no antibiotic is produced, but the resistance functions, encoded by carFG, are expressed from the internal promoter (Pint). At high cell densities (bottom), a high concentration of 3-oxo-C6-HSL is achieved and CarR binds 3-oxo-C6-HSL, making it competent to activate transcription of the carA-H genes from PQS and also to upregulate its own transcription. As a result, Car antibiotic is produced. The regulator Hor is also required for carA-H expression and other regulatory inputs are indicated: carI expression is dependent on carbon source and possibly also downregulated in the presence of high 3-oxo-C6-HSL levels; temperature affects hor transcription and probably also affects carI expression on a posttranscriptional level. Arrows with “+” indicate positive regulation, and flattened arrowhead indicates repression. Refer to text and references 13 and 33 for details.
Model for the regulation of virulence factor production by AHL QS in E. carotovora. At low cell density (top), ExpI synthesizes the AHL signaling molecule, 3-oxo-C6-HSL, which diffuses into the environment. VirR, the cognate LuxR homologue, is expressed constitutively and may directly repress expression of PCWDEs. RsmA is activated by VirR and itself represses expression of rsmB and PCWDEs. At high cell density, high concentrations of 3-oxo-C6 HSL are achieved and the signal binds to VirR. This causes derepression and allows expression of PCWDEs and rsmB. The untranslated RNA rsmB further sequesters RsmA in the cell, thus immediately affecting PCWDE expression in a cell-density-dependent manner.