ArticleLife science alliance2019
Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress.
Article in Life science alliance, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Native entanglement misfolding contributes to age-associated structural changebioRxiv : the preprint server for biology · 2026Article
- Chaperone regulation of biomolecular condensates.Frontiers in biophysics · 2024Article
- Regulation of germline proteostasis by HSF1 and insulin/IGF-1 signaling.Biochemical Society transactions · 2023Article
- Verification of the Interaction Target Protein of the Effector ApCE22 ofBiomolecules · 2023Article
- Genome-Wide Identification of Aquaporin Genes in Adzuki Bean (International journal of molecular sciences · 2022Article
- Mad3 modulates the GScience advances · 2022Article
- Modeling aging and its impact on cellular function and organismal behavior.Experimental gerontology · 2021Review
- Profiling the physiological pitfalls of anti-hepatitis C direct-acting agents in budding yeast.Microbial biotechnology · 2021Article
- Stress granules display bistable dynamics modulated by Cdk.The Journal of cell biology · 2021Article
- The budding yeast Start repressor Whi7 differs in regulation from Whi5, emerging as a major cell cycle brake in response to stress.Journal of cell science · 2020Article
- Proteostasis collapse, a hallmark of aging, hinders the chaperone-Start network and arrests cells in G1.eLife · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The precise coordination of growth and proliferation has a universal prevalence in cell homeostasis. As a prominent property, cell size is modulated by the coordination between these processes in bacterial, yeast, and mammalian cells, but the underlying molecular mechanisms are largely unknown. Here, we show that multifunctional chaperone systems play a concerted and limiting role in cell-cycle entry, specifically driving nuclear accumulation of the G1 Cdk-cyclin complex. Based on these findings, we establish and test a molecular competition model that recapitulates cell-cycle-entry dependence on growth rate. As key predictions at a single-cell level, we show that availability of the Ydj1 chaperone and nuclear accumulation of the G1 cyclin Cln3 are inversely dependent on growth rate and readily respond to changes in protein synthesis and stress conditions that alter protein folding requirements. Thus, chaperone workload would subordinate Start to the biosynthetic machinery and dynamically adjust proliferation to the growth potential of the cell.
Indexed as
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What OpenQuestion holds
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.