Yeast infectious protein (prion) forms of the Ure2 and Sup35 proteins determine the nonchromosomal genes [URE3] and [PSI], and these are, therefore, the basis for a kind of epigenetic phenomena. In many systems, introduction of multiple copies of a DNA gene, or dsRNA copies of its sequence, results in the epigenetic silencing of that gene. In parallel with these homology effects, which act at the level of DNA or RNA, elevated copy number of the Ure2 and Sup35 proteins increases the frequency of their own "silencing" by prion formation. Both [URE3] and [PSI] appear to be due to self-propagating-amyloid formation of Ure2p and Sup35p, respectively. Another prion, [Het-s] of the filamentous fungus, Podospora anserina, is necessary for a normal cellular function, heterokaryon incompatibility. Since these prions are nonchromosomal genes, they are proteins acting as genes, a parallel to the fact that nucleic acids can catalyze enzymatic reactions.
|Evidence ID||Analyze ID||Interactor||Interactor Systematic Name||Interactor||Interactor Systematic Name||Type||Assay||Annotation||Action||Modification||Phenotype||Source||Reference||Note|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Gene Ontology Term||Gene Ontology Term ID||Qualifier||Aspect||Method||Evidence||Source||Assigned On||Annotation Extension||Reference|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Phenotype||Experiment Type||Experiment Type Category||Mutant Information||Strain Background||Chemical||Details||Reference|
|Evidence ID||Analyze ID||Regulator||Regulator Systematic Name||Target||Target Systematic Name||Experiment||Assay||Construct||Conditions||Strain Background||Reference|