The genetic structure of a global sample of 170 clinical and nonclinical Saccharomyces cerevisiae isolates was analysed using 12 microsatellite markers. High levels of genetic diversity were revealed both among the clinical and among the nonclinical S. cerevisiae isolates without significant differentiation between these two groups of isolates, rendering a single origin of pathogenic isolates unlikely. This suggests that S. cerevisiae is a true opportunistic pathogen, with a diversity of unrelated genetic backgrounds able to cause infections in humans, and that the ability of S. cerevisiae isolates to cause infections is likely due to a combination of their phenotypic plasticity and the immune system status of the exposed individuals. As was previously reported for bread, beer and wine strains and for environmental S. cerevisiae isolates, the microsatellite genotypes indicated ploidy level variation, from possibly haploid up to tetraploid, among clinical S. cerevisiae isolates. However, rather than haploid, sporulation proficiency and spore viability data indicated that most S. cerevisiae isolates that were mono-allelic at all examined microsatellite loci were likely homothallic and self-diploidized. Interestingly, the proportion of heterozygous clinical isolates was found to be significantly higher than the proportion of heterozygous nonclinical isolates, suggesting a selective advantage of heterozygous S. cerevisiae yeasts in clinical environments.
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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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Evidence ID | Analyze ID | File | Description |
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