system, the first to be described, comprises the lasR gene coding for the LasR
regulatory protein and the lasI gene coding for an enzyme, autoinducer
synthase, LasI, which is necessary for the synthesis of a type of AHL: N-
(3-oxododecanoyl) -L-homoserine lactone (3-oxo-C12-HSL). As in V. ficheri,
3-oxo-C12-HSL have the property of easily crossing bacterial membranes and thus
constitute a real means of communication between bacteria. When the
3-oxo-C12-HSL concentration reaches a critical, high bacterial concentration
threshold, one AHL molecule binds to two LasR proteins to form an activator
complex for the transcription of several genes. This activation is triggered
synchronously throughout the bacterial population at the junction between the
exponential growth phase and the beginning of the stationary phase. The genes
activated by this system include:
• lasB, lasA, aprA coding respectively for two elastases, and for an
alkaline protease each contributing to the destruction of the lung tissues,
• toxA, coding for an ADP-ribosylating exotoxin,
• xcpR and xcpP, coding for proteins of the type II secretion machinery
required for export.
these factors outside the bacterium,
• and lasI,
allowing a rapid increase in the synthesis of 3-oxo-C12-HSL and therefore an
amplification of signal by self-induction.
The second system rhl operates according to the
same scheme and comprises the rhlR gene, coding for the regulatory protein RhlR
and the rhlI gene, coding for an autoinducer synthase enzyme, RhlI required for
the synthesis of a second type of AHL: N-butyryl L-homoserine lactone (C4-HSL).
The RhlR-C4-HS1 complex controls the expression of the rhlAB operon required
for the production of rhamnolipid, and the expression of a series of genes
including lasB, lasA, aprA, and rhlI. several other QS-regulated genes were
identified in three studies using a transcriptional analysis approach of the P.
aeruginosa genome and DNA microarray technology. The majority of
transcripts regulated by QS would translate proteins whose functions are
hypothetical or even unknown. Ninety-seven genes are found in common in all
three studies. To confirm the validity of these results, it will be necessary
to identify and characterize these proteins Despite
the structural similarity between the activator/inductor couples (LasR/LasI and
RhlR/RhlI) of the two systems, none of the components of one system can replace
those of the other. However, there are interactions between these two systems.
The LasR-3-oxo-C12-HSL complex activates the transcription of rhlR and rhlI. In
addition, 3-oxo-C12-HSL may compete with C4-HSL for the RhlI binding site and
thus may act as an antagonism of the rhl system. So, there is a hierarchy
between these two systems with the las system which positively regulates the