Quorum sensing (QS) is a cell-cell communication mechanism mediated by secreted hormone-like signaling molecules that operates in both Gram-positive and Gram-negative bacteria, driving coordinated alterations in gene expression once a critical cell density is reached. In these prokaryotic systems, bacteria produce, release, detect, and respond to small autoinducers, such as acyl-homoserine lactones in Gram-negative bacteria, oligopeptides in Gram-positive bacteria, and the universal autoinducer-2, to regulate community behaviors including biofilm formation, virulence factor production, and stress adaptation. The concept of QS in eukaryotic microbes emerged decades ago, and later investigations confirmed that unicellular fungi and protozoa similarly measure population density to regulate collective activities. In Saccharomyces cerevisiae, aromatic alcohols (2-phenylethanol, tryptophol, tyrosol) serve as QS signals to control filamentous growth, biofilm assembly, and environmental stress responses. Candida albicans employs farnesol to suppress hyphal development while utilizing tyrosol to accelerate germ tube emergence and biofilm maturation. African trypanosomes, including Trypanosoma brucei and related species, generate oligopeptides via secreted peptidases that accumulate as stumpy induction factors (SIFs), triggering a density-dependent shift from proliferative slender forms to transmission-competent stumpy forms essential for tsetse fly infection. QS-based mechanisms influence virulence factors in fungal and protozoan pathogens, affecting their ability to colonize hosts. Exploring QS in eukaryotic organisms opens new possibilities for antifungal treatments and parasite management. By interfering with QS signaling, researchers can disrupt fungal biofilm formation and regulate protozoan development, paving the way for innovative disease control methods.
Mohammadzadeh et al. (Sat,) studied this question.