288
A. V. Ravi et al.
6 Quorum Sensing in Vibrios
Two general types of QS systems have been reported in Vibrios, depending on
whether the signals molecules are detected in the cytoplasm or at the cell surface. The
former group involves the QS systems that use N-acylhomoserine lactones (AHLs) as
signal molecules. These systems are found in many Gram-negative aquatic bacterial
pathogens, including A. hydrophila and A. salmonicida. The latter group of system
is multi-lingual QS system as found in vibrios, such as the aquaculture pathogens V.
harveyi, V. anguillarum and V. vulnificus.
In vibrios, QS is the phenomenon of multi-channel gene expression system
synchronized by three different types of autoinducers. The LuxM/N QS system
utilizes AHLs as signal molecules, whereas CqsA/S system utilizes CAI-1 (“Cholera
autoinducer -1”), and in the third QS system, the signal molecules are together
referred as autoinducer-2 (AI-2) (Milton 2006). Third QS system appears to be
shared by many Gram-positive and Gram-negative species and is based on a mixture
of inter convertible molecules collectively referred as autoinducer-2 (AI-2). A crucial
enzyme in the production of AI-2 is LuxS. LuxS directs the breakdown of Sribosylhomocysteine to homocysteine and 4,5-dihydroxy-2,3-pentanedione (DPD).
Not all QS systems are present in Vibrio spp., because most of them contain the AI-2
based QS system. In Vibrio spp., AI-2 binds to LuxP, a periplasmic AI-2 receptor that
is connected with the LuxQ sensor kinase-phosphatase. However, at higher population density, AI-2 will bind to LuxP and as a result LuxQ will act as a phosphatase,
leading to a dephosphorylation of LuxO. Since, dephosphorylated LuxO became
quiet, no small regulatory RNAs will be formed and the LuxR mRNA remains stable,
resulting in the production of LuxR and ultimately an altered gene expression pattern
(Fig. 1; Table 1).
AI-2 based QS play an important role in regulating the secretion of several virulence factors, biofilm formation and stress responses in several Vibrio spp. In aquatic
bacterial pathogens, the QS circuits, like AI-1 and AI-2 control the genes responsible for bioluminescence, conjugation, motility, sporulation, biocorrosion, antibiotic production, most importantly biofilm formation and the expression of virulence
factors such as lytic enzymes, toxins, siderophores and adhesion molecules (de Kievit
and Iglewski 2000; de Windt et al. 2003).
Moreover, in vibrios, QS mediated phenotypic factors including virulence factors
production and biofilm formation plays a vital role in causing diseases in animals
(Randall et al. 2004). These signal molecules are known to coordinate the production
of virulence factors and biofilm formation in response to the cell density of the
surrounding bacterial population (You et al. 2007; Yildiz and Visick 2009). The
biofilm forming potential of Vibrio spp. is responsible for their survival, virulence
and stress resistance (Packiavathy et al. 2013). Such biofilms are the preferable
lifestyle for bacteria as they colonize and enhance growth and survival by affording
the free entry to nutrients and develop resistant to antibiotics. It has also been found
that bacteria remains vegetative within the biofilm often up to 1000 fold more tougher
to antibiotics, chemicals and heavy metals than free swimming cells. It was reported
A. V. Ravi et al.
6 Quorum Sensing in Vibrios
Two general types of QS systems have been reported in Vibrios, depending on
whether the signals molecules are detected in the cytoplasm or at the cell surface. The
former group involves the QS systems that use N-acylhomoserine lactones (AHLs) as
signal molecules. These systems are found in many Gram-negative aquatic bacterial
pathogens, including A. hydrophila and A. salmonicida. The latter group of system
is multi-lingual QS system as found in vibrios, such as the aquaculture pathogens V.
harveyi, V. anguillarum and V. vulnificus.
In vibrios, QS is the phenomenon of multi-channel gene expression system
synchronized by three different types of autoinducers. The LuxM/N QS system
utilizes AHLs as signal molecules, whereas CqsA/S system utilizes CAI-1 (“Cholera
autoinducer -1”), and in the third QS system, the signal molecules are together
referred as autoinducer-2 (AI-2) (Milton 2006). Third QS system appears to be
shared by many Gram-positive and Gram-negative species and is based on a mixture
of inter convertible molecules collectively referred as autoinducer-2 (AI-2). A crucial
enzyme in the production of AI-2 is LuxS. LuxS directs the breakdown of Sribosylhomocysteine to homocysteine and 4,5-dihydroxy-2,3-pentanedione (DPD).
Not all QS systems are present in Vibrio spp., because most of them contain the AI-2
based QS system. In Vibrio spp., AI-2 binds to LuxP, a periplasmic AI-2 receptor that
is connected with the LuxQ sensor kinase-phosphatase. However, at higher population density, AI-2 will bind to LuxP and as a result LuxQ will act as a phosphatase,
leading to a dephosphorylation of LuxO. Since, dephosphorylated LuxO became
quiet, no small regulatory RNAs will be formed and the LuxR mRNA remains stable,
resulting in the production of LuxR and ultimately an altered gene expression pattern
(Fig. 1; Table 1).
AI-2 based QS play an important role in regulating the secretion of several virulence factors, biofilm formation and stress responses in several Vibrio spp. In aquatic
bacterial pathogens, the QS circuits, like AI-1 and AI-2 control the genes responsible for bioluminescence, conjugation, motility, sporulation, biocorrosion, antibiotic production, most importantly biofilm formation and the expression of virulence
factors such as lytic enzymes, toxins, siderophores and adhesion molecules (de Kievit
and Iglewski 2000; de Windt et al. 2003).
Moreover, in vibrios, QS mediated phenotypic factors including virulence factors
production and biofilm formation plays a vital role in causing diseases in animals
(Randall et al. 2004). These signal molecules are known to coordinate the production
of virulence factors and biofilm formation in response to the cell density of the
surrounding bacterial population (You et al. 2007; Yildiz and Visick 2009). The
biofilm forming potential of Vibrio spp. is responsible for their survival, virulence
and stress resistance (Packiavathy et al. 2013). Such biofilms are the preferable
lifestyle for bacteria as they colonize and enhance growth and survival by affording
the free entry to nutrients and develop resistant to antibiotics. It has also been found
that bacteria remains vegetative within the biofilm often up to 1000 fold more tougher
to antibiotics, chemicals and heavy metals than free swimming cells. It was reported