About this Research Topic
Quorum-sensing (QS) allows bacteria to share information about cell density to adjust gene expression accordingly. This cell-cell communication relies on secreted signal molecules, called autoinducers or pheromones, which are predominantely peptides in Gram-positive bacteria. This system enables bacteria to undergo energetically expensive processes as a collective only when the impact of these processes on their environment is more likely to be efficient.
Genetic and structure/function analysis of both signaling peptide and cognate sensor regulator led to the characterization of the major Gram-positive signaling pathways which can be divided into two groups depending on the mode of action of the peptide. The signaling peptides can either act on the outside of the cell or in the cytoplasm. In the former case, detection of the peptide pheromone relies on membrane embedded histidine-kinases of two-component systems. Pheromone binding stimulates autophosphorylation of the histidine–kinase and transfer of the phosphoryl group to a cytoplasmic response regulator. Once activated, the response regulator is able to bind DNA and control the transcription of target genes. Agr-type and gly-gly peptides systems belong to this group. In the latter case, these communication systems, which have been more extensively studied in the last few years, are mediated by re-internalized signaling peptides that directly interact with cytoplasmic sensors. Most of these sensors act as transcriptional regulators and are called direct QS sensors. The RNPP family and the Rgg-like regulatory family belong to this group.
Among the many traits controlled by cell-cell communication is the expression of virulence factors. Quenching microbial QS or, in short, quorum quenching, is a promising strategy that may allow the control of infection by interfering with cell-cell communication using small inhibiting molecules. This should attenuate adaptation to the host environment rather than inhibit cell growth. Except for strategies that have been investigated to inhibit the two-component QS system Agr of Staphylococcus, the design of molecules modulating QS systems in other Gram-positive pathogenic bacteria has been poorly explored.
Recent advances in the field indicate that cell-cell communication via autoinducers occurs both within and between bacterial species and reports also show that signaling peptides are able to activate non-cognate regulators. Furthermore, the genomes of Gram-positive bacteria harbor small CDS that encode peptides of unknown function. This suggests that peptide pheromones might control more bacterial processes than we imagine.
In this Research Topic, we wish to give an overview of the advances concerning newly discovered, as well as already known, QS mechanisms. Questions we consider include -but are not restricted to- quorum-quenching, cross-talk between peptides and regulators, identification of signaling peptides. The presentation of reviews, methods (genetic, biochemical, bioinformatic analysis, single cell and in vivo (insect or mammal) models) and ongoing original works describing all these different aspect of QS systems is greatly encouraged.
Genetic and structure/function analysis of both signaling peptide and cognate sensor regulator led to the characterization of the major Gram-positive signaling pathways which can be divided into two groups depending on the mode of action of the peptide. The signaling peptides can either act on the outside of the cell or in the cytoplasm. In the former case, detection of the peptide pheromone relies on membrane embedded histidine-kinases of two-component systems. Pheromone binding stimulates autophosphorylation of the histidine–kinase and transfer of the phosphoryl group to a cytoplasmic response regulator. Once activated, the response regulator is able to bind DNA and control the transcription of target genes. Agr-type and gly-gly peptides systems belong to this group. In the latter case, these communication systems, which have been more extensively studied in the last few years, are mediated by re-internalized signaling peptides that directly interact with cytoplasmic sensors. Most of these sensors act as transcriptional regulators and are called direct QS sensors. The RNPP family and the Rgg-like regulatory family belong to this group.
Among the many traits controlled by cell-cell communication is the expression of virulence factors. Quenching microbial QS or, in short, quorum quenching, is a promising strategy that may allow the control of infection by interfering with cell-cell communication using small inhibiting molecules. This should attenuate adaptation to the host environment rather than inhibit cell growth. Except for strategies that have been investigated to inhibit the two-component QS system Agr of Staphylococcus, the design of molecules modulating QS systems in other Gram-positive pathogenic bacteria has been poorly explored.
Recent advances in the field indicate that cell-cell communication via autoinducers occurs both within and between bacterial species and reports also show that signaling peptides are able to activate non-cognate regulators. Furthermore, the genomes of Gram-positive bacteria harbor small CDS that encode peptides of unknown function. This suggests that peptide pheromones might control more bacterial processes than we imagine.
In this Research Topic, we wish to give an overview of the advances concerning newly discovered, as well as already known, QS mechanisms. Questions we consider include -but are not restricted to- quorum-quenching, cross-talk between peptides and regulators, identification of signaling peptides. The presentation of reviews, methods (genetic, biochemical, bioinformatic analysis, single cell and in vivo (insect or mammal) models) and ongoing original works describing all these different aspect of QS systems is greatly encouraged.
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