Yeasts produce numerous antimicrobial agents such as killer toxins, volatile organic compounds (VOCs), and other secondary metabolites, establishing themselves in developing natural and sustainable biocontrol strategies for agriculture and food preservation. This study addressed the biocontrol potential of yeasts, isolated from spontaneous fermentations of rosehips (Rosa canina L.) and rowanberries (Sorbus aucuparia L.), focusing on their killer phenotypes and VOCs production. Yeasts were isolated using spontaneous fermentations with Hanseniaspora uvarum and Metschnikowia pulcherrima identified as the dominant species, comprising approximately 70% of the yeast population. Among 163 isolated strains, 20% demonstrated killing activity, with Saccharomyces cerevisiae exhibiting the strongest killing efficiency, as well as Pichia anomala and M. pulcherrima showing broad-spectrum antagonistic activity. This study identified dsRNA-encoded killer phenotypes in S. cerevisiae, S. paradoxus, and Torulaspora delbrueckii, revealing multiple distinct killer toxin types. The biocontrol potential of wild berry-inhabiting yeasts was demonstrated in a real food system, grape juice, where the S. cerevisiae K2-type killer strain significantly reduced fungal contaminants. The selected H. uvarum, M. pulcherrima, S. cerevisiae, and S. paradoxus yeast strains representing both berries were applied for VOC analysis and identification by gas chromatography-linked mass spectrometry. It was revealed that the patterns of emitted volatiles are yeast species-specific. Statistically significant differences between the individual VOCs were observed among killing phenotype-possessing vs. non-killer S. paradoxus yeasts, thus revealing the involvement of killer systems in multi-level biocontrol enablement. The performed studies deepen our understanding of potential yeast biocontrol mechanisms, highlight the importance of produced antimicrobials and volatiles in ensuring antagonistic efficacy, and prove the relevance of isolated biocontrol yeasts for improving food safety.
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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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| 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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