Abstract
Bacterial cell-cell communication or quorum sensing (QS) is a biological process commonly described as allowing bacteria belonging to a same pherotype to coordinate gene expression to cell density. In Gram-positive bacteria, cell-cell communication mainly relies on cytoplasmic sensors regulated by secreted and re-imported signaling peptides. The Bacillus quorum sensors Rap, NprR, and PlcR were previously identified as the first members of a new protein family called RNPP. Except for the Rap proteins, these RNPP regulators are transcription factors that directly regulate gene expression. QS regulates important biological functions in bacteria of the Bacillus cereus group. PlcR was first characterized as the main regulator of virulence in B. thuringiensis and B. cereus. More recently, the PlcR-like regulator PlcRa was characterized for its role in cysteine metabolism and in resistance to oxidative stress. The NprR regulator controls the necrotrophic properties allowing the bacteria to survive in the infected host. The Rap proteins negatively affect sporulation via their interaction with a phosphorelay protein involved in the activation of Spo0A, the master regulator of this differentiation pathway. In this review we aim at providing a complete picture of the QS systems that are sequentially activated during the lifecycle of B. cereus and B. thuringiensis in an insect model of infection.
Highlights
Bacillus thuringiensis produces insect-specific delta-endotoxins that form a crystal in the bacterium during growth under nutrient starvation [1]
It was shown that the B. thuringiensis genome contains a set of genes induced after the insect death [15]. Expression of these genes, encoding degradative enzymes, such as metalloproteases, lipases, and chitinases, and the enzymatic machinery synthesizing the lipopeptide kurstakin, depends on the transcription activator NprR. This regulator is responsible for the necrotrophic behavior of B. thuringiensis in its host as an nprR deletion mutant does not survive in the insect cadaver
The role, regulation and interconnection of these RNPP quorum sensing (QS) systems in B. thuringiensis during infection of insect larvae will be the focus of this review
Summary
Bacillus thuringiensis produces insect-specific delta-endotoxins (or Cry proteins) that form a crystal in the bacterium during growth under nutrient starvation [1]. CytK, Hbl and Nhe were linked to toxi-infections with a diarrheic syndrome [5] The genes encoding these proteins are under the control of the transcription regulator PlcR and belong to the PlcR regulon [12]. Expression of these genes, encoding degradative enzymes, such as metalloproteases, lipases, and chitinases, and the enzymatic machinery synthesizing the lipopeptide kurstakin, depends on the transcription activator NprR This regulator is responsible for the necrotrophic behavior of B. thuringiensis in its host as an nprR deletion mutant does not survive in the insect cadaver. Intracellular acting AIP are internalized in the cell via an oligopeptide permease system They will bind to a sensor thereby affecting its activity as a transcriptional regulator or rendering it inactive by disrupting its interaction with another protein. The role, regulation and interconnection of these RNPP QS systems in B. thuringiensis during infection of insect larvae will be the focus of this review
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