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.
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| Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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| Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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| Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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| Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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| Site | Modification | Modifier | Source | Reference |
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| Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Increase the total number of rows showing on this page by using the pull-down located below the table, or use the page scroll at the table's top right to browse through the table's pages; use the arrows to the right of a column header to sort by that column; filter the table using the "Filter" box at the top of the table; click on the small "i" buttons located within a cell for an annotation to view further details about experiment type and any other genes involved in the interaction.
| Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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| Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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| Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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