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

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  • 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)

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.

Suggested Citation

  • Yi-Hu Dong & Lian-Hui Wang & Jin-Ling Xu & Hai-Bao Zhang & Xi-Fen Zhang & Lian-Hui Zhang, 2001. "Quenching quorum-sensing-dependent bacterial infection by an N-acyl homoserine lactonase," Nature, Nature, vol. 411(6839), pages 813-817, June.
    • Handle: RePEc:nat:nature:v:411:y:2001:i:6839:d:10.1038_35081101
    DOI: 10.1038/35081101
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    Cited by:

    1. Woo-Suk Jung & Jeehyun Lee & Myung-Il Kim & Jun Ma & Tomohisa Nagamatsu & Eunhye Goo & Hongsup Kim & Ingyu Hwang & Jaehong Han & Sangkee Rhee, 2011. "Structural and Functional Analysis of Phytotoxin Toxoflavin-Degrading Enzyme," PLOS ONE, Public Library of Science, vol. 6(7), pages 1-9, July.
    2. Lisa Thoenen & Marco Kreuzer & Christine Pestalozzi & Matilde Florean & Pierre Mateo & Tobias Züst & Anlun Wei & Caitlin Giroud & Liza Rouyer & Valentin Gfeller & Matheus D. Notter & Eva Knoch & Siegf, 2024. "The lactonase BxdA mediates metabolic specialisation of maize root bacteria to benzoxazinoids," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    3. Evgeni V Nikolaev & Eduardo D Sontag, 2016. "Quorum-Sensing Synchronization of Synthetic Toggle Switches: A Design Based on Monotone Dynamical Systems Theory," PLOS Computational Biology, Public Library of Science, vol. 12(4), pages 1-33, April.

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