ReviewMicrobiology and molecular biology reviews : MMBR1999
Prions in Saccharomyces and Podospora spp.: protein-based inheritance.
Review in Microbiology and molecular biology reviews : MMBR, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 73 citations in OpenAlex.
- Amyloids and prions in the light of evolution.Current genetics · 2023Review
- MIL-CELL: a tool for multi-scale simulation of yeast replication and prion transmission.European biophysics journal : EBJ · 2023Article
- Overview of the Special Issue "Protein-Based Infection, Inheritance, and Memory".International journal of molecular sciences · 2023Article
- All-atom simulation of the HET-s prion replication.PLoS computational biology · 2020Article
- Asparagine and glutamine ladders promote cross-species prion conversion.The Journal of biological chemistry · 2017Article
- Prions and the concept of polyprionic inheritance.Current genetics · 2017Review
- Review
- Fungal prion HET-s as a model for structural complexity and self-propagation in prions.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Heterogeneous seeding of a prion structure by a generic amyloid form of the fungal prion-forming domain HET-s(218-289).The Journal of biological chemistry · 2013Article
- Degradation of fungal prion HET-s(218-289) induces formation of a generic amyloid fold.Biophysical journal · 2012Article
- A small, glutamine-free domain propagates the [SWI(+)] prion in budding yeast.Molecular and cellular biology · 2011Article
- A new colour assay for [URE3] prion in a genetic background used to score for the [PSI⁺] prion.Yeast (Chichester, England) · 2011Article
- Analysis of Paramecium tetraurelia A-51 surface antigen gene mutants reveals positive-feedback mechanisms for maintenance of expression and temperature-induced activation.Eukaryotic cell · 2005Article
- Genetic interactions between [PSI+] and nonstop mRNA decay affect phenotypic variation.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Use of yeast as a model system to investigate protein conformational diseases.Molecular biotechnology · 2005Review
- Het up mould unleashes a sporekiller prion.Journal of biosciences · 2003Article
- Sexual transmission of the [Het-S] prion leads to meiotic drive in Podospora anserina.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- A fratricidal fungal prion.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Conservation of a portion of the S. cerevisiae Ure2p prion domain that interacts with the full-length protein.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Nonself recognition is mediated by HET-C heterocomplex formation during vegetative incompatibility.The EMBO journal · 2002Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Genetic evidence showed two non-Mendelian genetic elements of Saccharomyces cerevisiae, called [URE3] and [PSI], to be prions of Ure2p and Sup35p, respectively. [URE3] makes cells derepressed for nitrogen catabolism, while [PSI] elevates the efficiency of weak suppressor tRNAs. The same approach led to identification of the non-Mendelian element [Het-s] of the filamentous fungus Podospora anserina, as a prion of the het-s protein. The prion form of the het-s protein is required for heterokaryon incompatibility, a normal fungal function, suggesting that other normal cellular functions may be controlled by prions. [URE3] and [PSI] involve a self-propagating aggregation of Ure2p and Sup35p, respectively. In vitro, Ure2p and Sup35p form amyloid, a filamentous protein structure, high in beta-sheet with a characteristic green birefringent staining by the dye Congo Red. Amyloid deposits are a cardinal feature of Alzheimer's disease, non-insulin-dependent diabetes mellitus, the transmissible spongiform encephalopathies, and many other diseases. The prion domain of Ure2p consists of Asn-rich residues 1 to 80, but two nonoverlapping fragments of the molecule can, when overproduced, induce the de nova appearance of [URE3]. The prion domain of Sup35 consists of residues 1 to 114, also rich in Asn and Gln residues. While runs of Asn and Gln are important for [URE3] and [PSI], no such structures are found in PrP or the Het-s protein. Either elevated or depressed levels of the chaperone Hsp104 interfere with propagation of [PSI]. Both [URE3] and [PSI] are cured by growth of cells in millimolar guanidine HCl. [URE3] is also cured by overexpression of fragments of Ure2p or fusion proteins including parts of Ure2p.
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