Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 98, Issue 5, Pages 2752-2757Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.051624298
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- NIGMS NIH HHS [GM59026, R01 GM059026] Funding Source: Medline
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The opportunistic pathogenic bacterium Pseudomonas aeruginosa uses quorum-sensing signaling systems as global regulators of virulence genes. There are two quorum-sensing signal receptor and signal generator pairs, LasR-Lasl and RhlR-Rhll. The recently completed P. aeruginosa genome-sequencing project revealed a gene coding for a homolog of the signal receptors, LasR and RhlR. Here we describe a role for this gene, which we call qscR. The qscR gene product governs the timing of quorum-sensing-controlled gene expression and it dampens virulence in an insect model. We present evidence that suggests the primary role of QscR is repression of lasl. A qscR mutant produces the Lasl-generated signal prematurely, and this results in premature transcription of a number of quorum-sensing-regulated genes. When fed to Drosophila melanogaster, the qscR mutant kills the animals more rapidly than the parental P. aeroginosa. The repression of lasl by QscR could serve to ensure that quorum-sensing-controlled genes are not activated in environments where they are not useful.
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