ArticleProceedings of the National Academy of Sciences of the United States of America2001
Protein misfolding and temperature up-shift cause G1 arrest via a common mechanism dependent on heat shock factor in Saccharomycescerevisiae.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 108 citations in OpenAlex.
- Mistranslating tRNA variants impact the proteome and phosphoproteome of Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2026Article
- Mechanosensor-mediated Hsp70 phosphorylation orchestrates the landscape of the heat shock response.Nature communications · 2025Article
- The endoplasmic reticulum-associated degradation machinery selectively degrades stress-induced TIN1 during stress recovery.Plant physiology · 2025Article
- Mistranslating tRNA variants impact the proteome and phosphoproteome ofbioRxiv : the preprint server for biology · 2025Article
- Hsf1 is essential for proteotoxic stress response in smyd1b-deficient embryos and fish survival under heat shock.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Diverse yeast antiviral systems prevent lethal pathogenesis caused by the L-A mycovirus.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Inducible transcriptional condensates drive 3D genome reorganization in the heat shock response.Molecular cell · 2022Article
- Regulating Expression of Mistranslating tRNAs by Readthrough RNA Polymerase II Transcription.ACS synthetic biology · 2021Article
- Cell adaptation to aneuploidy by the environmental stress response dampens induction of the cytosolic unfolded-protein response.Molecular biology of the cell · 2021Article
- A highly conserved mechanism for the detoxification and assimilation of the toxic phytoproduct L-azetidine-2-carboxylic acid in Aspergillus nidulans.Scientific reports · 2021Article
- SPAAC Pulse-Chase: A Novel Click Chemistry-Based Method to Determine the Half-Life of Cellular Proteins.Frontiers in cell and developmental biology · 2021Article
- The prefoldin complex stabilizes the von Hippel-Lindau protein against aggregation and degradation.PLoS genetics · 2020Article
- Precise Replacement ofG3 (Bethesda, Md.) · 2020Article
- Growth-Regulated Hsp70 Phosphorylation Regulates Stress Responses and Prion Maintenance.Molecular and cellular biology · 2020Article
- Proline Homeostasis inFrontiers in genetics · 2020Review
- Causative Links between Protein Aggregation and Oxidative Stress: A Review.International journal of molecular sciences · 2019Review
- Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress.Life science alliance · 2019Article
- Heterologous Hsp90 promotes phenotypic diversity through network evolution.PLoS biology · 2018Article
- Loss of mRNA surveillance pathways results in widespread protein aggregation.Scientific reports · 2018Article
- The ribosomal DNA metaphase loop of Saccharomyces cerevisiae gets condensed upon heat stress in a Cdc14-independent TORC1-dependent manner.Cell cycle (Georgetown, Tex.) · 2018Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of misfolded proteins in the cell at high temperature may cause entry into a nonproliferating, heat-shocked state. The imino acid analog azetidine 2-carboxylic acid (AZC) is incorporated into cellular protein competitively with proline and can misfold proteins into which it is incorporated. AZC addition to budding yeast cells at concentrations sufficient to inhibit proliferation selectively activates heat shock factor (HSF). We find that AZC treatment fails to cause accumulation of glycogen and trehalose (Msn2/4-dependent processes) or to induce thermotolerance (a protein kinase C-dependent process). However, AZC-arrested cells can accumulate glycogen and trehalose and can acquire thermotolerance in response to a subsequent heat shock. We find that AZC treatment arrests cells in a viable state and that this arrest is reversible. We find that cells at high temperature or cells deficient in the ubiquitin-conjugating enzymes Ubc4 and Ubc5 are hypersensitive to AZC-induced proliferation arrest. We find that AZC treatment mimics temperature up-shift in arresting cells in G1 and represses expression of CLN1 and CLN2. Mutants with reduced G1 cyclin-Cdc28 activity are hypersensitive to AZC-induced proliferation arrest. Expression of the hyperstable Cln3-2 protein prevents G1 arrest upon AZC treatment and temperature up-shift. Finally, we find that the EXA3-1 mutation, encoding a defective HSF, prevents efficient G1 arrest in response to both temperature up-shift and AZC treatment. We conclude that nontoxic levels of misfolded proteins (induced by AZC treatment or by high temperature) selectively activate HSF, which is required for subsequent G1 arrest.
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