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Bacteria and fungi ubiquitously coexist, with their interactions critically influencing human health and industrial processes. Quorum sensing (QS) is a core regulatory mechanism that enables density-dependent coordination and phenotypic responses across these two kingdoms. While bacteria and fungi utilize their respective QS systems to engage in competitive or cooperative interactions to enhance their environmental adaptability, the current understanding of QS-based communications between them remains scattered, and a systematic summary of this field is still lacking. In this review, we examine the intricate dialog between bacteria and fungi, focusing on its role in microbial network assembly and ecosystem function, to provide a comprehensive analysis and engineering perspective on QS-based cross-kingdom communication. Specifically, we will first briefly delineate the core architecture of bacterial and fungal QS systems and the phenotypes they govern. Then, we will analyze QS-based interactions across diverse environments between different bacteria and fungi, categorizing natural QS interactions based on various phenotypes, including biofilm co-assembly and metabolic complementation. We further compare and analyze synthetic biology strategies, including promoter engineering and directed evolution of QS regulatory components, for reprogramming bacterial-fungal interactions and their applications. By synthesizing and contrasting these natural paradigms with synthetic designs, we provide a blueprint for achieving modular control over bacterial-fungal communities in diverse environments. Finally, by outlining persistent challenges and future trends, we aim to propel this field forward, enabling the deciphering of complex microbial interactions and ultimately increasing our capacity to engineer microbial consortia for diverse applications.

SmcR family proteins were discovered in the 1990s as central regulators of quorum-sensing gene expression and later discovered to be conserved in all studied Vibrio species. SmcR homologs regulate a wide range of genes involved in pathogenesis, including but not limited to genes involved in biofilm production and toxin secretion. As archetypal members of the broad class of TetR-type transcription factors, each SmcR-type protein has a predicted ligand-binding pocket. However, no native ligand has been identified for these proteins that control their function as regulators. Here, we used SmcR-specific chemical inhibitors to determine that ligand binding drives proteolytic degradation in vivo , providing the first demonstration of SmcR function connected to ligand binding for this historical protein family.

Understanding the social structure and evolutionary dynamics of microbial communities requires the identification and characterization of relevant mutant subpopulations. While employs quorum sensing (QS) to coordinate population-wide behaviors, the social traits of many QS mutants remain poorly defined. In this study, we developed an iterative \"targeted gene duplication followed by mutant screening\" (TGD-MS) approach to systematically identify noncanonical QS cheater mutants. We discovered that a single-nucleotide mutation in , which encodes the α subunit of RNA polymerase (RNAP), produces a QS-deficient phenotype resembling QS-null mutants. This RpoA variant mutant exhibits characteristic features of social cheating, including a competitive growth advantage in mixed populations, impaired QS-dependent virulence factor production, and attenuated pathogenicity. Structural and biochemical analyses revealed that the RpoA variant impairs RNAP binding to the promoters of core QS genes ( and ), leading to diminished QS activity. Further examination of natural RpoA variants uncovered a spectrum of QS-related phenotypes, suggesting that RpoA has a dual regulatory role in QS control. Within the C-terminal domain (α-CTD) of RpoA, we identified two distinct functional determinants that, through adaptive mutations, can acquire opposing regulatory effects on QS. This enables an environmentally dependent phenotypic switch between cooperation and cheating. Our discovery of noncanonical RpoA-mediated QS cheaters expands the framework of bacterial social evolution, demonstrating that mutations outside the canonical QS circuitry can disrupt cooperative behaviors. These findings underscore how core transcriptional machinery can be evolutionarily co-opted to modulate complex social interactions in dynamic environments.IMPORTANCETo understand how bacterial populations function and evolve, it is essential to identify socially significant subpopulations, including previously unrecognized types of cheaters. In this study, we uncover an unexpected role of RNA polymerase (RNAP) in regulating quorum sensing (QS) and QS-associated social behaviors in . Specifically, we demonstrate that the α subunit of RNAP (RpoA) is a key regulatory component in this process. A single-nucleotide mutation within the C-terminal domain of RpoA was found to alter QS activity, driving an environment-dependent transition between cooperative and cheating phenotypes. This discovery of this novel, noncanonical QS cheater mutant offers new insights into intra-population interactions, population stability, and evolutionary dynamics. These findings carry significant implications for microbial ecology and deepen our understanding of social evolution in bacterial communities.

Quorum sensing (QS) enables bacteria such as Pseudomonas aeruginosa to coordinate cooperative activities. How bacteria in cooperating groups can resist infiltration by non-cooperating variants is an emerging area of interest in sociobiology and molecular biology. There have been several recent reports on how QS and certain bacteriophage interact. In some strains of P. aeruginosa , QS can activate phage defense systems. At least one bacteriophage can repress P. aeruginosa QS. Here, we show that a previously undescribed bacteriophage can help cooperating groups of P. aeruginosa resist infiltration by non-cooperating QS mutants. This represents a mutualism in which both the bacteriophage and the P. aeruginosa host benefit at least under certain conditions.

The theory of persisting independent and isolated regarding microorganisms is no longer accepted. To survive and reproduce they have developed several communication platforms within the cells which facilitates them to adapt the surrounding environmental changes. This cell-to-cell communication is termed as quorum sensing; it relies upon the cell density and can stimulate several traits of microbes including biofilm formation, competence, and virulence factors secretion. Initially, this sophisticated mode of communication was discovered in bacteria; later, it was also confirmed in eukaryotes (fungi). As a consequence, many quorum-sensing molecules and inhibitors have been identified and characterized in various fungal species. In this review article, we will primarily focus on fungal quorum-sensing molecules and the production of inhibitors from fungal species with potential applications for combating fungal infections.

The discovery of quorum-sensing responsive linear plasmid phages has transformed understanding of phage-bacterial interactions by demonstrating inter-domain chemical communication. To date, however, examples of quorum-sensing responsive phages have been sparse. The founding example of such a phage, φVP882, detects a chemical communication signal molecule called DPO that is produced by diverse bacterial species. We investigated whether a family of VP882-like phages might exist that detect and respond to DPO. We find that indeed, VP882-like phages reside in DPO-producing bacterial species isolated at different times and geographic locations, suggesting their wide circulation in the environment. This discovery strengthens the evidence for the generality of phage-bacterial inter-domain chemical communication.

Bacteria interact with both abiotic and biotic factors in their environment. Quorum sensing (QS) is one mechanism that bacteria use to communicate with other bacteria and coordinate behaviors in the population. QS regulates a wide variety of processes ranging from the production of light to the modulation of virulence factors; some bacteria use single QS circuits, whereas others have several. The opportunistic pathogen Pseudomonas aeruginosa uses QS to control some virulence functions and has three complete QS circuits. Our study explores why bacteria might have multiple QS circuits. We show how a non-QS regulated factor, MexT, influences QS regulators in P. aeruginosa, and we uncover the diversity of QS architectures in clinical isolates. These studies begin to reveal the benefits (or disadvantages) of multiple QS circuits, allowing us to understand the behaviors of bacteria that have a range of implications in health, agriculture, and bioremediation.

Vibrio parahaemolyticus is a major global cause of seafood-associated gastroenteritis, relying on its tightly controlled T3SS1 for virulence. While the quorum sensing regulators AphA and OpaR are known to modulate T3SS1, the full regulatory network remains incompletely understood. This study identifies two novel transcription factors, TftR (TetR family) and VltR (LysR family), that fine-tune T3SS1 activity through distinct mechanisms. These findings reveal a multilayered regulatory hierarchy that enables V. parahaemolyticus to precisely calibrate virulence in response to cell density and environmental cues. Understanding these regulatory interactions provides new insights into bacterial pathogenesis and may guide the development of targeted antivirulence strategies against this clinically important pathogen.

This Review highlights how we can build upon the relatively new and rapidly developing field of research into bacterial quorum sensing (QS). We now have a depth of knowledge about how bacteria use QS signals to communicate with each other and to coordinate their activities. In recent years there have been extraordinary advances in our understanding of the genetics, genomics, biochemistry, and signal diversity of QS. We are beginning to understand the connections between QS and bacterial sociality. This foundation places us at the beginning of a new era in which researchers will be able to work towards new medicines to treat devastating infectious diseases, and use bacteria to understand the biology of sociality. A Review of the genetics, biochemistry, ecology and evolution of bacterial quorum sensing. Bacterial communication Bacterial quorum sensing is a strategy for regulating gene expression that orchestrates collective group behaviour. In this Review, Peter Greenberg and colleagues explore the progress that has been made in understanding bacterial quorum sensing, including the genetics, biochemistry and ecology of these systems, which are used by bacteria to communicate and to coordinate their behaviour. They also discuss the future outlook for this field in terms of understanding sociality in bacteria, and how these systems could be used to develop antibacterial agents.

CRISPR-Cas are prokaryotic adaptive immune systems that provide protection against bacteriophage (phage) and other parasites. Little is known about how CRISPR-Cas systems are regulated, preventing prediction of phage dynamics in nature and manipulation of phage resistance in clinical settings. Here, we show that the bacterium Pseudomonas aeruginosa PA14 uses the cell–cell communication process, called quorum sensing, to activate cas gene expression, to increase CRISPR-Cas targeting of foreign DNA, and to promote CRISPR adaptation, all at high cell density. This regulatory mechanism ensures maximum CRISPR-Cas function when bacterial populations are at highest risk for phage infection. We demonstrate that CRISPR-Cas activity and acquisition of resistance can be modulated by administration of proand antiquorum-sensing compounds. We propose that quorum-sensing inhibitors could be used to suppress the CRISPR-Cas adaptive immune system to enhance medical applications, including phage therapies.