Quenching quorum-sensing-dependent bacterial infection by an N-acyl homoserine lactonase

Yi-Hu Dong, Lian-Hui Wang, Jin-Ling Xu, Hai-Bao Zhang, Xi-Fen Zhang and Lian-Hui Zhang ()
Additional contact information
Yi-Hu Dong: Laboratory of Biosignals and Bioengineering, Institute of Molecular Agrobiology, National University of Singapore
Lian-Hui Wang: Laboratory of Biosignals and Bioengineering, Institute of Molecular Agrobiology, National University of Singapore
Jin-Ling Xu: Laboratory of Biosignals and Bioengineering, Institute of Molecular Agrobiology, National University of Singapore
Hai-Bao Zhang: Laboratory of Biosignals and Bioengineering, Institute of Molecular Agrobiology, National University of Singapore
Xi-Fen Zhang: Laboratory of Biosignals and Bioengineering, Institute of Molecular Agrobiology, National University of Singapore
Lian-Hui Zhang: Laboratory of Biosignals and Bioengineering, Institute of Molecular Agrobiology, National University of Singapore

Nature, 2001, vol. 411, issue 6839, 813-817

Abstract: 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 sensing1,2. 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 pathogens3,4,5,6,7,8,9. AHL-producing tobacco restored the pathogenicity of an AHL-negative mutant of Erwinia carotovora10. 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.11, 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.

Date: 2001
References: Add references at CitEc
Citations: View citations in EconPapers (3)

Downloads: (external link)
https://www.nature.com/articles/35081101 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:411:y:2001:i:6839:d:10.1038_35081101

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/35081101

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().