ArticlePLoS genetics2009
Loss of yeast peroxiredoxin Tsa1p induces genome instability through activation of the DNA damage checkpoint and elevation of dNTP levels.
Article in PLoS genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 43 citations in OpenAlex.
- The multiple activations in budding yeast S-phase checkpoint are Poisson processes.PNAS nexus · 2023Article
- Peroxiredoxin, Senescence, and Cancer.Cells · 2022Review
- Effects of Serine or Threonine in the Active Site of Typical 2-Cys Prx on Hyperoxidation Susceptibility and on Chaperone Activity.Antioxidants (Basel, Switzerland) · 2021Article
- The Peroxiredoxin Asp f3 Acts as Redox Sensor inGenes · 2021Article
- Piecing Together How Peroxiredoxins Maintain Genomic Stability.Antioxidants (Basel, Switzerland) · 2018Review
- Peroxiredoxin Involvement in the Initiation and Progression of Human Cancer.Antioxidants & redox signaling · 2018Review
- Pathways and Mechanisms that Prevent Genome Instability inGenetics · 2017Review
- Article
- Article
- Microbial 2-Cys Peroxiredoxins: Insights into Their Complex Physiological Roles.Molecules and cells · 2016Review
- Leveraging DNA damage response signaling to identify yeast genes controlling genome stability.G3 (Bethesda, Md.) · 2015Article
- Loss of APD1 in yeast confers hydroxyurea sensitivity suppressed by Yap1p transcription factor.Scientific reports · 2015Article
- Thiol peroxidase deficiency leads to increased mutational load and decreased fitness in Saccharomyces cerevisiae.Genetics · 2014Article
- The yeast peroxiredoxin Tsa1 protects against protein-aggregate-induced oxidative stress.Journal of cell science · 2014Article
- Loss of the thioredoxin reductase Trr1 suppresses the genomic instability of peroxiredoxin tsa1 mutants.PloS one · 2014Article
- Cotranscriptional recruitment of yeast TRAMP complex to intronic sequences promotes optimal pre-mRNA splicing.Nucleic acids research · 2014Article
- Article
- A chemostat array enables the spatio-temporal analysis of the yeast proteome.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- miRNA and TMPRSS2-ERG do not mind their own business in prostate cancer cells.Immunogenetics · 2013Review
- Global analysis of SUMO chain function reveals multiple roles in chromatin regulation.The Journal of cell biology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peroxiredoxins are a family of antioxidant enzymes critically involved in cellular defense and signaling. Particularly, yeast peroxiredoxin Tsa1p is thought to play a role in the maintenance of genome integrity, but the underlying mechanism is not understood. In this study, we took a genetic approach to investigate the cause of genome instability in tsa1Delta cells. Strong genetic interactions of TSA1 with DNA damage checkpoint components DUN1, SML1, and CRT1 were found when mutant cells were analyzed for either sensitivity to DNA damage or rate of spontaneous base substitutions. An elevation in intracellular dNTP production was observed in tsa1Delta cells. This was associated with constitutive activation of the DNA damage checkpoint as indicated by phosphorylation of Rad9/Rad53p, reduced steady-state amount of Sml1p, and induction of RNR and HUG1 genes. In addition, defects in the DNA damage checkpoint did not modulate intracellular level of reactive oxygen species, but suppressed the mutator phenotype of tsa1Delta cells. On the contrary, overexpression of RNR1 exacerbated this phenotype by increasing dNTP levels. Taken together, our findings uncover a new role of TSA1 in preventing the overproduction of dNTPs, which is a root cause of genome instability.
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.