ArticleeLife2019
Proteostasis collapse, a hallmark of aging, hinders the chaperone-Start network and arrests cells in G1.
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
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- Native entanglement misfolding contributes to age-associated structural changebioRxiv : the preprint server for biology · 2026Article
- Cell enlargement drives aging-associated proteome remodeling and shortens replicative lifespan.bioRxiv : the preprint server for biology · 2026Article
- Cdc42 interacts with chaperone Ydj1 to enhance its stability and partitioning during asymmetric cell division and aging in yeast.PLoS biology · 2026Article
- Gerobiotics: Exploring the Potential and Limitations of Repurposing Probiotics in Addressing Aging Hallmarks and Chronic Diseases.Probiotics and antimicrobial proteins · 2026Review
- Hsp70 chaperones, Ssa1 and Ssa2, limit poly(A) binding protein aggregation.Molecular biology of the cell · 2025Article
- Sis2 regulates yeast replicative lifespan in a dose-dependent manner.Nature communications · 2023Article
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- Senescence in yeast is associated with amplified linear fragments of chromosome XII rather than ribosomal DNA circle accumulation.PLoS biology · 2023Article
- Artificial Hsp104-mediated systems for re-localizing protein aggregates.Nature communications · 2023Article
- Damage dynamics and the role of chance in the timing of E. coli cell death.Nature communications · 2023Article
- Chaperone-Dependent Degradation of Cdc42 Promotes Cell Polarity and Shields the Protein from Aggregation.Molecular and cellular biology · 2023Article
- Therapeutic Antiaging Strategies.Biomedicines · 2022Review
- A rare natural lipid induces neuroglobin expression to prevent amyloid oligomers toxicity and retinal neurodegeneration.Aging cell · 2022Article
- Mad3 modulates the GScience advances · 2022Article
- Contribution of Infrared Spectroscopy to the Understanding of Amyloid Protein Aggregation in Complex Systems.Frontiers in molecular biosciences · 2022Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 4 countries.
Funding
Abstract
Loss of proteostasis and cellular senescence are key hallmarks of aging, but direct cause-effect relationships are not well understood. We show that most yeast cells arrest in G1 before death with low nuclear levels of Cln3, a key G1 cyclin extremely sensitive to chaperone status. Chaperone availability is seriously compromised in aged cells, and the G1 arrest coincides with massive aggregation of a metastable chaperone-activity reporter. Moreover, G1-cyclin overexpression increases lifespan in a chaperone-dependent manner. As a key prediction of a model integrating autocatalytic protein aggregation and a minimal Start network, enforced protein aggregation causes a severe reduction in lifespan, an effect that is greatly alleviated by increased expression of specific chaperones or cyclin Cln3. Overall, our data show that proteostasis breakdown, by compromising chaperone activity and G1-cyclin function, causes an irreversible arrest in G1, configuring a molecular pathway postulating proteostasis decay as a key contributing effector of cell senescence.
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Registered trials
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.