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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.

Bacterial quorum sensing enables control of collective behaviors. In Vibrio cholerae , the DPO-VqmA-VqmR quorum-sensing circuit governs key processes, including biofilm formation. Here, we identify a double-negative feedback loop between the transcription factor LuxT and the small RNA VqmR. This regulatory circuit depends on an eight amino acid N-terminal region that exists only in V. cholerae LuxT and LuxT from its close relatives. This short peptide sequence confers three distinct functions: it enables LuxT to repress vqmR , renders luxT mRNA susceptible to VqmR repression, and governs which DNA motifs LuxT can bind. Our findings reveal a pathogen-specific regulatory module that links small RNA targeting of mRNAs to transcription factor DNA binding specificity. The results show how evolution tailors bacterial regulatory circuits to adapt to different environments.

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.

To 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 P. aeruginosa . 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.

Pseudomonas aeruginosa is an opportunistic human pathogen that causes infections in the most vulnerable, immunocompromised patient population. Additionally, P. aeruginosa infections are notoriously hard to treat with even the strongest antibiotics available in the clinic. P. aeruginosa relies heavily on its communication mechanism, quorum sensing, in order to stage infections. The quorum sensing system presents an ideal opportunity for the discovery of new antibiotics that are effective in treating P. aeruginosa infections. The work here presents new tools for the development of antibiotics targeting a key protein-protein interaction of the P. aeruginosa quorum-sensing system. The molecules, methods, and insights described here will be of great value in the discovery of anti-quorum-sensing therapies against a pathogen that presents a formidable threat to human health.

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.