Halogenated furanones inhibit quorum sensing through accelerated LuxR turnover

Research output: Contribution to journal › Journal article › Research › peer-review

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Halogenated furanones inhibit quorum sensing through accelerated LuxR turnover. / Manefield, Michael; Rasmussen, Thomas Bovbjerg; Henzter, Morten; Andersen, Jens Bo; Steinberg, Peter; Kjelleberg, Staffan; Givskov, Michael.

In: Microbiology, Vol. 148, No. Pt 4, 2002, p. 1119-27.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Manefield, M, Rasmussen, TB, Henzter, M, Andersen, JB, Steinberg, P, Kjelleberg, S & Givskov, M 2002, 'Halogenated furanones inhibit quorum sensing through accelerated LuxR turnover', Microbiology, vol. 148, no. Pt 4, pp. 1119-27.

APA

Manefield, M., Rasmussen, T. B., Henzter, M., Andersen, J. B., Steinberg, P., Kjelleberg, S., & Givskov, M. (2002). Halogenated furanones inhibit quorum sensing through accelerated LuxR turnover. Microbiology, 148(Pt 4), 1119-27.

Vancouver

Manefield M, Rasmussen TB, Henzter M, Andersen JB, Steinberg P, Kjelleberg S et al. Halogenated furanones inhibit quorum sensing through accelerated LuxR turnover. Microbiology. 2002;148(Pt 4):1119-27.

Author

Manefield, Michael ; Rasmussen, Thomas Bovbjerg ; Henzter, Morten ; Andersen, Jens Bo ; Steinberg, Peter ; Kjelleberg, Staffan ; Givskov, Michael. / Halogenated furanones inhibit quorum sensing through accelerated LuxR turnover. In: Microbiology. 2002 ; Vol. 148, No. Pt 4. pp. 1119-27.

Bibtex

@article{ec17aecbeab74a59a1557ce23cf7eeee,
title = "Halogenated furanones inhibit quorum sensing through accelerated LuxR turnover",
abstract = "N-acyl-L-homoserine lactones (AHLs) are co-regulatory ligands required for control of the expression of genes encoding virulence traits in many Gram-negative bacterial species. Recent studies have indicated that AHLs modulate the cellular concentrations of LuxR-type regulatory proteins by binding and fortifying these proteins against proteolytic degradation (Zhu & Winans, 2001 ). Halogenated furanones produced by the macroalga Delisea pulchra inhibit AHL-dependent gene expression. This study assayed for an in vivo interaction between a tritiated halogenated furanone and the LuxR protein of Vibrio fischeri overproduced in Escherichia coli. Whilst a stable interaction between the algal metabolite and the bacterial protein was not found, it was noted by Western analysis that the half-life of the protein is reduced up to 100-fold in the presence of halogenated furanones. This suggests that halogenated furanones modulate LuxR activity but act to destabilize, rather than protect, the AHL-dependent transcriptional activator. The furanone-dependent reduction in the cellular concentration of the LuxR protein was associated with a reduction in expression of a plasmid encoded P(luxI)-gfp(ASV) fusion suggesting that the reduction in LuxR concentration is the mechanism by which furanones control expression of AHL-dependent phenotypes. The mode of action by which halogenated furanones reduce cellular concentrations of the LuxR protein remains to be characterized.",
keywords = "Escherichia coli, Furans, Gene Expression Regulation, Bacterial, Kinetics, Repressor Proteins, Structure-Activity Relationship, Trans-Activators, Vibrio",
author = "Michael Manefield and Rasmussen, {Thomas Bovbjerg} and Morten Henzter and Andersen, {Jens Bo} and Peter Steinberg and Staffan Kjelleberg and Michael Givskov",
year = "2002",
language = "English",
volume = "148",
pages = "1119--27",
journal = "Microbiology",
issn = "1350-0872",
publisher = "Society for General Microbiology",
number = "Pt 4",

}

RIS

TY - JOUR

T1 - Halogenated furanones inhibit quorum sensing through accelerated LuxR turnover

AU - Manefield, Michael

AU - Rasmussen, Thomas Bovbjerg

AU - Henzter, Morten

AU - Andersen, Jens Bo

AU - Steinberg, Peter

AU - Kjelleberg, Staffan

AU - Givskov, Michael

PY - 2002

Y1 - 2002

N2 - N-acyl-L-homoserine lactones (AHLs) are co-regulatory ligands required for control of the expression of genes encoding virulence traits in many Gram-negative bacterial species. Recent studies have indicated that AHLs modulate the cellular concentrations of LuxR-type regulatory proteins by binding and fortifying these proteins against proteolytic degradation (Zhu & Winans, 2001 ). Halogenated furanones produced by the macroalga Delisea pulchra inhibit AHL-dependent gene expression. This study assayed for an in vivo interaction between a tritiated halogenated furanone and the LuxR protein of Vibrio fischeri overproduced in Escherichia coli. Whilst a stable interaction between the algal metabolite and the bacterial protein was not found, it was noted by Western analysis that the half-life of the protein is reduced up to 100-fold in the presence of halogenated furanones. This suggests that halogenated furanones modulate LuxR activity but act to destabilize, rather than protect, the AHL-dependent transcriptional activator. The furanone-dependent reduction in the cellular concentration of the LuxR protein was associated with a reduction in expression of a plasmid encoded P(luxI)-gfp(ASV) fusion suggesting that the reduction in LuxR concentration is the mechanism by which furanones control expression of AHL-dependent phenotypes. The mode of action by which halogenated furanones reduce cellular concentrations of the LuxR protein remains to be characterized.

AB - N-acyl-L-homoserine lactones (AHLs) are co-regulatory ligands required for control of the expression of genes encoding virulence traits in many Gram-negative bacterial species. Recent studies have indicated that AHLs modulate the cellular concentrations of LuxR-type regulatory proteins by binding and fortifying these proteins against proteolytic degradation (Zhu & Winans, 2001 ). Halogenated furanones produced by the macroalga Delisea pulchra inhibit AHL-dependent gene expression. This study assayed for an in vivo interaction between a tritiated halogenated furanone and the LuxR protein of Vibrio fischeri overproduced in Escherichia coli. Whilst a stable interaction between the algal metabolite and the bacterial protein was not found, it was noted by Western analysis that the half-life of the protein is reduced up to 100-fold in the presence of halogenated furanones. This suggests that halogenated furanones modulate LuxR activity but act to destabilize, rather than protect, the AHL-dependent transcriptional activator. The furanone-dependent reduction in the cellular concentration of the LuxR protein was associated with a reduction in expression of a plasmid encoded P(luxI)-gfp(ASV) fusion suggesting that the reduction in LuxR concentration is the mechanism by which furanones control expression of AHL-dependent phenotypes. The mode of action by which halogenated furanones reduce cellular concentrations of the LuxR protein remains to be characterized.

KW - Escherichia coli

KW - Furans

KW - Gene Expression Regulation, Bacterial

KW - Kinetics

KW - Repressor Proteins

KW - Structure-Activity Relationship

KW - Trans-Activators

KW - Vibrio

M3 - Journal article

C2 - 11932456

VL - 148

SP - 1119

EP - 1127

JO - Microbiology

JF - Microbiology

SN - 1350-0872

IS - Pt 4

ER -

ID: 44310098