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Impact of quorum sensing on fitness of Pseudomonas aeruginosaInternational Journal of Medical Microbiology, Vol. 296, No. 2-3. (06 April 2006), pp. 93-102.
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AbstractIn Pseudomonas aeruginosa , cell–cell communication based on N -acyl-homoserine lactone (AHL) signal molecules (termed quorum sensing) is known to control the production of extracellular virulence factors. Hence, in pathogenic interactions with host organisms, the quorum-sensing (QS) machinery can confer a selective advantage on P. aeruginosa . However, as shown by transcriptomic and proteomic studies, many intracellular metabolic functions are also regulated by quorum sensing. Some of these serve to regenerate the AHL precursors methionine and S -adenosyl-methionine and to degrade adenosine via inosine and hypoxanthine. The fact that a significant percentage of clinical and environmental isolates of P. aeruginosa is defective for QS because of mutation in the major QS regulatory gene lasR , raises the question of whether the QS machinery can have a negative impact on the organism's fitness. In vitro, lasR mutants have a higher probability to escape lytic death in stationary phase under alkaline conditions than has the QS-proficient wild type. Similar selective forces might also operate in natural environments.
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