ArticleCurrent biology : CB2018
Decoupling Yeast Cell Division and Stress Defense Implicates mRNA Repression in Translational Reallocation during Stress.
Article in Current biology : CB, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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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
36 citing papers in PubMed, 56 citations in OpenAlex.
- HOG Signaling: A Multifunctional Regulator of Stress Homeostasis inJournal of fungi (Basel, Switzerland) · 2026Review
- Twenty-Five Years of the Environmental Stress Response and the Enduring Power of Yeast in Stress Biology.Yeast (Chichester, England) · 2026Review
- The importance of regulated resource reallocation during dynamic environmental shifts in yeast.The EMBO journal · 2026Article
- Surprising regulatory plasticity for the conserved HOG pathway in diversebioRxiv : the preprint server for biology · 2025Article
- Dynamic phosphorylation of Hcm1 promotes fitness in chronic stress.PLoS genetics · 2025Article
- Growth arrest is a DNA damage protection strategy in Arabidopsis.Nature communications · 2025Article
- Hog1/p38 regulates the integrated stress response (ISR) and global transcriptomic changes inbioRxiv : the preprint server for biology · 2025Article
- Dynamic phosphorylation of Hcm1 promotes fitness in chronic stress.bioRxiv : the preprint server for biology · 2025Article
- Transcriptional heterogeneity shapes stress-adaptive responses in yeast.Nature communications · 2025Article
- Article
- Dual regulation of the levels and function of Start transcriptional repressors drives G1 arrest in response to cell wall stress.Cell communication and signaling : CCS · 2025Article
- Regulated resource reallocation is transcriptionally hard wired into the yeast stress response.bioRxiv : the preprint server for biology · 2024Article
- Article
- Gcn2 rescues reprogramming in the absence of Hog1/p38 signaling inbioRxiv : the preprint server for biology · 2024Article
- Human-Fungal Pathogen Interactions from the Perspective of Immunoproteomics Analyses.International journal of molecular sciences · 2024Review
- Advances inJournal of fungi (Basel, Switzerland) · 2023Review
- PKA regulatory subunit Bcy1 couples growth, lipid metabolism, and fermentation during anaerobic xylose growth in Saccharomyces cerevisiae.PLoS genetics · 2023Article
- Article
- The regulatory mechanism of the yeast osmoresponse under different glucose concentrations.iScience · 2023Article
- The environmental stress response regulates ribosome content in cell cycle-arrestedFrontiers in cell and developmental biology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Stress tolerance and rapid growth are often competing interests in cells. Upon severe environmental stress, many organisms activate defense systems concurrent with growth arrest. There has been debate as to whether aspects of the stress-activated transcriptome are regulated by stress or an indirect byproduct of reduced proliferation. For example, stressed Saccharomyces cerevisiae cells mount a common gene expression program called the environmental stress response (ESR) [1] comprised of ∼300 induced (iESR) transcripts involved in stress defense and ∼600 reduced (rESR) mRNAs encoding ribosomal proteins (RPs) and ribosome biogenesis factors (RiBi) important for division. Because ESR activation also correlates with reduced growth rate in nutrient-restricted chemostats and prolonged G1 in slow-growing mutants, an alternate proposal is that the ESR is simply a consequence of reduced division [2-5]. A major challenge is that past studies did not separate effects of division arrest and stress defense; thus, the true responsiveness of the ESR-and the purpose of stress-dependent rESR repression in particular-remains unclear. Here, we decoupled cell division from the stress response by following transcriptome, proteome, and polysome changes in arrested cells responding to acute stress. We show that the ESR cannot be explained by changes in growth rate or cell-cycle phase during stress acclimation. Instead, failure to repress rESR transcripts reduces polysome association of induced transcripts, delaying production of their proteins. Our results suggest that stressed cells alleviate competition for translation factors by removing mRNAs and ribosomes from the translating pool, directing translational capacity toward induced transcripts to accelerate protein production.
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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.