Autoregulation of luxR: the Vibrio harveyi lux-operon activator functions as a repressor

Authors

  • Jaidip Chatterjee,

    1. Department of Biochemistry, McIntyre Medical Sciences Building, McGill University, 3655 Drummond Street, Montreal, Quebec, Canada H3G 1Y6.
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  • Carol M. Miyamoto,

    1. Department of Biochemistry, McIntyre Medical Sciences Building, McGill University, 3655 Drummond Street, Montreal, Quebec, Canada H3G 1Y6.
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  • Edward A. Meighen

    Corresponding author
    1. Department of Biochemistry, McIntyre Medical Sciences Building, McGill University, 3655 Drummond Street, Montreal, Quebec, Canada H3G 1Y6.
    • *For correspondence. Tel (514) 398 7272; Fax (514) 398 7384.

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Summary

Mobility-shift assays have been used to demonstrate that the activator of the Vibrio harveyi lux operon, LuxR, binds independently, and with similar affinity, to two sites upstream of its own open reading frame. One site was located between 52 and 107 bp upstream of, and the other site in a region 25 bp downstream of, the transcriptional start site. The luxR promoter, in a transcriptional fusion with the chloramphenicol acetyl transferase (cat) gene, could readily be expressed in Escherichia coli as well as V. harveyi in the absence of LuxR. In both species, the presence of the luxR gene product resulted in repression of luxR promotion. These results show that LuxR directly regulates its own expression by functioning as an autorepressor. A mechanism for this repression is suggested by evidence showing that LuxR has a negative effect on RNA polymerase binding to the luxR promoter. In light of the fact that LuxR is also part of a regulatory family of repressors, the mechanism by which LuxR functions as a transcriptional activator of the lux operon has been re-examined.

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