In mammalian prion diseases, an abnormally folded, aggregated form of the prion protein (PrP(Sc)) appears to catalyze a conformational switch of its cellular isoform (PrP(C)) to an aggregated state. A similar prion-like phenomenon has been reported for the Saccharomyces cerevisiae translation termination factor Sup35p that can adopt a self-propagating conformation. We have compared aggregation propensities of chimeric proteins derived from the Sup35p prion domain NM and PrP in vitro and in the cytosol of mammalian cells. Sup35p-NM and PrP displayed strikingly different aggregation behaviors when expressed in mammalian cells, with NM remaining soluble and cytosolic PrP spontaneously aggregating due to the globular domain of PrP. When fused to PrP(90-230), Sup35p-M exhibited an inhibitory effect for nucleation but increased aggregate growth, potentially by facilitating recruitment of newly synthesized chimeric proteins into the growing aggregates. This effect, however, could, to some extent, be counteracted by the prion-forming region Sup35p-N, thereby increasing aggregate frequency. Interestingly, a lowered nucleation rate was also observed in the presence of the amino-terminal region of PrP, suggesting that Sup35p-M and PrP(23-90) share some biological function in prion protein assembly. Our results provide new insights into prion protein aggregation behaviors, demonstrating the impact of dynamic interactions between prion domains and suggesting that aggregation of yeast and mammalian prion proteins is strongly influenced by yet unidentified cellular conditions or factors.
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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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