Variation in pathology of human prion disease is believed to be caused, in part, by distinct conformations of aggregated protein resulting in different prion strains. Several prions also exist in yeast and maintain different self-propagating structures, referred to as prion variants. Investigation of the yeast prion [PSI(+)] has been instrumental in deciphering properties of prion variants and modeling the physical basis of their formation. Here, we describe the generation of specific variants of the [RNQ(+)] prion in yeast transformed with fibers formed in vitro in different conditions. The fibers of the Rnq1p prion-forming domain (PFD) that induce different variants in vivo have distinct biochemical properties. The physical basis of propagation of prion variants has been previously correlated to rates of aggregation and disaggregation. With [RNQ(+)] prion variants, we found that the prion variant does not correlate with the rate of aggregation as anticipated but does correlate with stability. Interestingly, we found that there are differences in the ability of the [RNQ(+)] prion variants to faithfully propagate themselves and to template the aggregation of other proteins. Incorporating the mechanism of variant formation elucidated in this study with that previously proposed for [PSI(+)] variants has provided a framework to separate general characteristics of prion variant properties from those specific to individual prion proteins.
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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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