ArticlePLoS biology2007
Hsp104-dependent remodeling of prion complexes mediates protein-only inheritance.
Article in PLoS biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed.
- Modelling human proteostasis and organelle homeostasis disorders in yeast and its application in drug discovery.FEMS yeast research · 2026Review
- Stress granules and protein aggregates reveal intracellular resource competition.bioRxiv : the preprint server for biology · 2025Article
- The middle domain of Hsp104 can ensure substrates are functional after processing.PLoS genetics · 2024Article
- Multiple aspects of amyloid dynamicsFrontiers in molecular neuroscience · 2024Article
- Understanding the link between the actin cytoskeleton and prion biology.PLoS pathogens · 2023Article
- Methionine Sulfoxide Reductases Suppress the Formation of the [Antioxidants (Basel, Switzerland) · 2023Article
- Article
- Hsp104 N-terminal domain interaction with substrates plays a regulatory role in protein disaggregation.The FEBS journal · 2022Article
- Disease-associated mutations within the yeast DNAJB6 homolog Sis1 slow conformer-specific substrate processing and can be corrected by the modulation of nucleotide exchange factors.Nature communications · 2022Article
- Beyond Amyloid Fibers: Accumulation, Biological Relevance, and Regulation of Higher-Order Prion Architectures.Viruses · 2022Review
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- Molecular determinants and modifiers of Matrin-3 toxicity, condensate dynamics, and droplet morphology.iScience · 2022Article
- The yeast molecular chaperone, Hsp104, influences transthyretin aggregate formation.Frontiers in molecular neuroscience · 2022Article
- Amyloid particles facilitate surface-catalyzed cross-seeding by acting as promiscuous nanoparticles.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The HSP110/HSP70 disaggregation system generates spreading-competent toxic α-synuclein species.The EMBO journal · 2020Article
- Nucleation seed size determines amyloid clearance and establishes a barrier to prion appearance in yeast.Nature structural & molecular biology · 2020Article
- A unifying model for the propagation of prion proteins in yeast brings insight into the [PSI+] prion.PLoS computational biology · 2020Article
- How and why to build a mathematical model: A case study using prion aggregation.The Journal of biological chemistry · 2020Review
- Article
- Calcium-responsive transactivator (CREST) toxicity is rescued by loss of PBP1/ATXN2 function in a novel yeast proteinopathy model and in transgenic flies.PLoS genetics · 2019Article
31 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors.
Funding
Abstract
Inheritance of phenotypic traits depends on two key events: replication of the determinant of that trait and partitioning of these copies between mother and daughter cells. Although these processes are well understood for nucleic acid-based genes, the mechanisms by which protein-only or prion-based genetic elements direct phenotypic inheritance are poorly understood. Here, we report a process crucial for inheritance of the Saccharomyces cerevisiae prion [PSI(+)], a self-replicating conformer of the Sup35 protein. By tightly controlling expression of a Sup35-GFP fusion, we directly observe remodeling of existing Sup35([PSI+]) complexes in vivo. This dynamic change in Sup35([PSI+]) is lost when the molecular chaperone Hsp104, a factor essential for propagation of all yeast prions, is functionally impaired. The loss of Sup35([PSI+]) remodeling by Hsp104 decreases the mobility of these complexes in the cytosol, creates a segregation bias that limits their transmission to daughter cells, and consequently diminishes the efficiency of conversion of newly made Sup35 to the prion form. Our observations resolve several seemingly conflicting reports on the mechanism of Hsp104 action and point to a single Hsp104-dependent event in prion propagation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.