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|Title:||Quenching quorum-sensing-dependent bacterial infection by an N-acyl homoserine lactonase||Authors:||Dong, Y.-H.
|Issue Date:||14-Jun-2001||Citation:||Dong, Y.-H., Wang, L.-H., Xu, J.-L., Zhang, H.-B., Zhang, X.-F., Zhang, L.-H. (2001-06-14). Quenching quorum-sensing-dependent bacterial infection by an N-acyl homoserine lactonase. Nature 411 (6839) : 813-817. ScholarBank@NUS Repository. https://doi.org/10.1038/35081101||Abstract:||Bacterial cells sense their population density through a sophisticated cell-cell communication system and trigger expression of particular genes when the density reaches a threshold. This type of gene regulation, which controls diverse biological functions including virulence, is known as quorum sensing. Quorum-sensing signals, such as acyl-homoserine lactones (AHLs), are the essential components of the communication system. AHLs regulate virulence gene expression in a range of plant and animal (including human) bacterial pathogens. AHL-producing tobacco restored the pathogenicity of an AHL-negative mutant of Erwinia carotovora. Different bacterial species may produce different AHLs, which vary in the length and substitution of the acyl chain but contain the same homoserine lactone moiety. Here we show that the acyl-homoserine lactonase (AHL-lactonase), a new enzyme from Bacillus sp., inactivates AHL activity by hydrolysing the lactone bond of AHLs. Plants expressing AHL-lactonase quenched pathogen quorum-sensing signalling and showed significantly enhanced resistance to E. carotovora infection. Our results highlight a promising potential to use quorum-sensing signals as molecular targets for disease control, thereby broadening current approaches for prevention of bacterial infections.||Source Title:||Nature||URI:||http://scholarbank.nus.edu.sg/handle/10635/66780||ISSN:||00280836||DOI:||10.1038/35081101|
|Appears in Collections:||Staff Publications|
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