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PMID:14507383
Citation |
Lupp, C, Urbanowski, M, Greenberg, EP and Ruby, EG (2003) The Vibrio fischeri quorum-sensing systems ain and lux sequentially induce luminescence gene expression and are important for persistence in the squid host. Mol. Microbiol. 50:319-31 |
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Abstract |
Bacterial quorum sensing using acyl-homoserine lactones (acyl-HSLs) as cell-density dependent signalling molecules is important for the transcriptional regulation of many genes essential in the establishment and the maintenance of bacteria-host associations. Vibrio fischeri, the symbiotic partner of the Hawaiian bobtail squid Euprymna scolopes, possesses two distinct acyl-HSL synthase proteins, LuxI and AinS. Whereas the cell density-dependent regulation of luminescence by the LuxI-produced signal is a well-described phenomenon, and its role in light organ symbiosis has been defined, little is known about the ain system. We have investigated the impact of the V. fischeri acyl-HSL synthase AinS on both luminescence and symbiotic colonization. Through phenotypic studies of V. fischeri mutants we have found that the AinS-signal is the predominant inducer of luminescence expression in culture, whereas the impact of the LuxI-signal is apparent only at the high cell densities occurring in symbiosis. Furthermore, our studies revealed that ainS regulates activities essential for successful colonization of E. scolopes, i.e. the V. fischeri ainS mutant failed to persist in the squid light organ. Mutational inactivation of the transcriptional regulator protein LuxO in the ainS mutant partially or completely reversed all the observed phenotypes, demonstrating that the AinS-signal regulates expression of downstream genes through the inactivation of LuxO. Taken together, our results suggest that the two quorum-sensing systems in V. fischeri, ain and lux, sequentially induce the expression of luminescence genes and possibly other colonization factors. |
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Keywords |
Animals; Bacterial Proteins/metabolism; Decapodiformes/microbiology; Gene Deletion; Gene Expression Regulation, Bacterial; Genes, Bacterial; Homoserine/analogs & derivatives; Luminescent Measurements; Mutagenesis, Insertional; Mutation; Signal Transduction/physiology; Symbiosis/physiology; Vibrio/genetics; Vibrio/growth & development; Vibrio/physiology |
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Significance
Annotations
Gene product | Qualifier | GO Term | Evidence Code | with/from | Aspect | Extension | Notes | Status |
---|---|---|---|---|---|---|---|---|
involved_in |
GO:0008218: bioluminescence |
ECO:0000315: mutant phenotype evidence used in manual assertion |
P |
Seeded From UniProt |
complete | |||
GO:0008218: bioluminescence |
ECO:0000315: |
P |
In Figure 3, ainS mutant failed to persist in the squid light organ. |
complete | ||||
GO:0007165: signal transduction |
ECO:0000315: |
P |
Table 3. Demonstrates how ainS mutants were unable to synthesize C8-HSL, preventing sufficient signalling to repress the LuxO repressor. This phenomenon resulted in a decrease in symbiotic luminescence. |
complete | ||||
involved_in |
GO:0008218: bioluminescence |
ECO:0000315: mutant phenotype evidence used in manual assertion |
P |
Seeded From UniProt |
complete | |||
GO:0008218: bioluminescence |
ECO:0000315: |
P |
In Figure 3, the luxO mutant resulted in an acceleration of the onset of luminescence in culture |
complete | ||||
See also
References
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