Page 2 Plant-Bacteria Interactions Edited by Iqbal Ahmad, John ...
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136j 7 Quorum Sensing in <strong>Bacteria</strong>: Potential in <strong>Plant</strong> Health Protection<br />
luxS (E.c), respectively; these are highly homologous to one another but not to any<br />
other identified gene, indicating that luxS genes define a new family of autoinducerproducing<br />
genes.<br />
Freeman et al. [86] showed that V. harveyi control light production using two parallel<br />
QS systems. It produces two autoinducers, AI-1 and AI-2, which are recognized <strong>by</strong><br />
cognatemembrane-boundtwo-componenthybridsensorkinasescalledluxNandluxQ,<br />
respectively.TheyhavealsoshowedthattheAI-1andLuxNhaveamuchgreatereffecton<br />
the level of LuxO phosphate and therefore on Lux expression than do AI-2 and LuxQ.<br />
LuxO functions as an activator protein via interaction with alternative sigma factor<br />
sigma 54. LuxO together with sigma 54 activates the expression of negative regulator of<br />
luminescence;phenotypesotherthanluxareregulated<strong>by</strong>LuxOandsigma54[87].Inthe<br />
same year, Miyamoto et al. [88] observed that LuxO is involved in control of luminescence<br />
in V. fischeri but luxO was stimulated <strong>by</strong> N-acyl-HSL autoinducer, indicating that<br />
luxO is part of a second signal transduction system controlling luminescence.<br />
McKnight et al. [89] revealed that a second type of intercellular signal is involved in<br />
lasB induction (elastase). This signal was identified as two heptyl-3-hydroxy-4quinolone,<br />
designated as Pseudomonas quinolone signal (PQS). Its production and<br />
bioactivity depend on the las and rhl QS system, respectively. This signal is not<br />
involved in sensing cell density. Zhang and Pierson [90] reported that a second QS<br />
system, CsaR–CsaI, is involved in regulating biosynthesis of cell surface components<br />
in P. aureofaciens 30–84. Smith et al. [91] described that QS of P. aeruginosa<br />
contribute to its pathogenesis both <strong>by</strong> regulating expression of virulence factors<br />
(exoenzymes and toxins) and <strong>by</strong> inducing inflammation. 3-oxo-C 12-HSL activates T<br />
cells to produce the inflammatory cytokine gamma interferon [91]. It also induces<br />
cyclooxygenase 2 (Cox-2) expressions. Sinorhizobium meliloti required exopolysaccharides<br />
(EPSs) for efficient invasion of root nodules on the host plant: alfalfa. S.<br />
meliloti ExpR activates transcription of genes involved in EPSII production in a<br />
density-dependent manner [92].<br />
von Bodman et al. [93] described how phytopathogenic bacteria have incorporated<br />
QSmechanisms intocomplexregulatorycascades thatcontrol genesfor pathogenicity<br />
and colonization of host surface. QS involves the production of extracellular polysaccharide-degradative<br />
enzymes, antibiotics, siderophores and pigments as well as Hrp<br />
protein secretion, Ti plasmid transfer, mobility, biofilm formation and epiphytic fitness.<br />
Wagner et al. [94] investigated global gene expression patterns modulated <strong>by</strong> QS<br />
regulons. Pseudomonas quinolone signal is also an integral component of the circuitry<br />
and is required for the production of rhl-dependent exoproduct at the onset of stationary<br />
phase [95]. Twenty novel QS-regulated proteins were identified, many of which are<br />
involved in iron utilization, suggesting a link between QS and the iron regulatory<br />
system. PhuP and HasR are components of the two distinct heme uptake systems<br />
present in P. aeruginosa, both proteins are positively regulated <strong>by</strong> QS cascade.<br />
McGrath et al. [96] reported that PQS production was dependent on the ratio of<br />
3-oxo-C12-HSL and C4-HSL, suggesting a regulatory balance between the QS systems.<br />
Juhas et al. [97] identified the gene PA2591 as a major virulence regulator,<br />
vqsR, in the QS hierarchy. Sircili et al. [98] reported that QS activates that expression<br />
of the lee genes in EPEC (enteropathogenic Escherichia coli) with QseA activating