ArticleMolecular biology of the cell2009
Arsenic toxicity to Saccharomyces cerevisiae is a consequence of inhibition of the TORC1 kinase combined with a chronic stress response.
Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Navigating heavy metal stress: emerging roles of TOR and SnRK signaling in plant tolerance.Frontiers in plant science · 2026Review
- Arsenic binds to nuclear transport factors and disrupts nucleocytoplasmic transport.Journal of cell science · 2025Article
- Direct binding of arsenicals to nuclear transport factors disrupts nucleocytoplasmic transport.bioRxiv : the preprint server for biology · 2025Article
- Multilevel Regulation of Membrane Proteins in Response to Metal and Metalloid Stress: A Lesson from Yeast.International journal of molecular sciences · 2024Review
- Mechanisms of genotoxicity and proteotoxicity induced by the metalloids arsenic and antimony.Cellular and molecular life sciences : CMLS · 2023Review
- Identification of novel arsenic resistance genes in yeast.MicrobiologyOpen · 2022Article
- Interactions with Arsenic: Mechanisms of Toxicity and Cellular Resistance in Eukaryotic Microorganisms.International journal of environmental research and public health · 2021Review
- Genome-wide imaging screen uncovers molecular determinants of arsenite-induced protein aggregation and toxicity.Journal of cell science · 2021Article
- Protective Effect of Dictyophora Polysaccharides on Sodium Arsenite-Induced Hepatotoxicity: A Proteomics Study.Frontiers in pharmacology · 2021Article
- Arsenic Exposure and Compromised Protein Quality Control.Chemical research in toxicology · 2020Review
- Functional genomic characterization of metallothioneins in brown trout (Salmo trutta L.). using synthetic genetic analysis.Scientific reports · 2019Article
- FlbA-Regulated GeneApplied and environmental microbiology · 2019Article
- A systematic assessment of chemical, genetic, and epigenetic factors influencing the activity of anticancer drug KP1019 (FFC14A).Oncotarget · 2017Article
- The nutrient transceptor/PKA pathway functions independently of TOR and responds to leucine and Gcn2 in a TOR-independent manner.FEMS yeast research · 2017Article
- Experimental Evolution Reveals Interplay between Sch9 and Polyploid Stability in Yeast.PLoS genetics · 2016Article
- Article
- Proteomic Analysis Identifies Ribosome Reduction as an Effective Proteotoxic Stress Response.The Journal of biological chemistry · 2015Article
- Impact of acute metal stress in Saccharomyces cerevisiae.PloS one · 2014Article
- Environmental signaling through the mechanistic target of rapamycin complex 1: mTORC1 goes nuclear.Cell cycle (Georgetown, Tex.) · 2014Review
- In scarcity and abundance: metabolic signals regulating cell growth.Physiology (Bethesda, Md.) · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The conserved Target Of Rapamycin (TOR) growth control signaling pathway is a major regulator of genes required for protein synthesis. The ubiquitous toxic metalloid arsenic, as well as mercury and nickel, are shown here to efficiently inhibit the rapamycin-sensitive TORC1 (TOR complex 1) protein kinase. This rapid inhibition of the TORC1 kinase is demonstrated in vivo by the dephosphorylation and inactivation of its downstream effector, the yeast S6 kinase homolog Sch9. Arsenic, mercury, and nickel cause reduction of transcription of ribosome biogenesis genes, which are under the control of Sfp1, a TORC1-regulated transcriptional activator. We report that arsenic stress deactivates Sfp1 as it becomes dephosphorylated, dissociates from chromatin, and exits the nucleus. Curiously, whereas loss of SFP1 function leads to increased arsenic resistance, absence of TOR1 or SCH9 has the opposite effect suggesting that TORC1 has a role beyond down-regulation of Sfp1. Indeed, we show that arsenic activates the transcription factors Msn2 and Msn4 both of which are targets of TORC1 and protein kinase A (PKA). In contrast to TORC1, PKA activity is not repressed during acute arsenic stress. A normal level of PKA activity might serve to dampen the stress response since hyperactive Msn2 will decrease arsenic tolerance. Thus arsenic toxicity in yeast might be determined by the balance between chronic activation of general stress factors in combination with lowered TORC1 kinase activity.
Indexed as
Identifiers
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.