ArticleMolecular biology of the cell2021
Cell adaptation to aneuploidy by the environmental stress response dampens induction of the cytosolic unfolded-protein response.
Article in Molecular biology of the cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Aneuploidy promotes transient stress adaptation and metabolic flexibility in the human fungal pathogen Aspergillus fumigatus.Current biology : CB · 2026Article
- Mitochondrial dysfunction in oocytes: implications for fertility and ageing.Journal of ovarian research · 2025Review
- Multilevel Gene Expression Changes in Lineages Containing Adaptive Copy Number Variants.Molecular biology and evolution · 2025Article
- Patterns of Aneuploidy and Signaling Consequences in Cancer.Cancer research · 2024Review
- Multilevel gene expression changes in lineages containing adaptive copy number variants.bioRxiv : the preprint server for biology · 2024Article
- Genetic inactivation of essentialMolecular biology of the cell · 2023Article
- Chromosomal Instability Causes Sensitivity to Polyamines and One-Carbon Metabolism.Metabolites · 2023Article
- The environmental stress response regulates ribosome content in cell cycle-arrestedFrontiers in cell and developmental biology · 2023Article
- Dynamic Features of Chromosomal Instability during Culture of Induced Pluripotent Stem Cells.Genes · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Aneuploid yeast cells are in a chronic state of proteotoxicity, yet do not constitutively induce the cytosolic unfolded protein response, or heat shock response (HSR) by heat shock factor 1 (Hsf1). Here, we demonstrate that an active environmental stress response (ESR), a hallmark of aneuploidy across different models, suppresses Hsf1 induction in models of single-chromosome gain. Furthermore, engineered activation of the ESR in the absence of stress was sufficient to suppress Hsf1 activation in euploid cells by subsequent heat shock while increasing thermotolerance and blocking formation of heat-induced protein aggregates. Suppression of the ESR in aneuploid cells resulted in longer cell doubling times and decreased viability in the presence of additional proteotoxicity. Last, we show that in euploids, Hsf1 induction by heat shock is curbed by the ESR. Strikingly, we found a similar relationship between the ESR and the HSR using an inducible model of aneuploidy. Our work explains a long-standing paradox in the field and provides new insights into conserved mechanisms of proteostasis with potential relevance to cancers associated with aneuploidy.
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