Evidence map›Paper›PMID 26344768›Full record

ArticleCell reports2015

Cross-Talk between Carbon Metabolism and the DNA Damage Response in S. cerevisiae.

Kobi J Simpson-Lavy, Alex Bronstein, Martin Kupiec, Mark Johnston

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. International journal of molecular sciences · 2022
    Review
  8. Article
  9. The Rad53Nature communications · 2020
    Article
  10. Article
  11. Review
  12. Article
  13. CaMolecular cell · 2019
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Spontaneous mutations inMicrobial cell (Graz, Austria) · 2018
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Kobi J Simpson-LavyUniversity of Colorado School of Medicine, Department of Biochemistry and Molecular Genetics, 12801 E 17(th) Avenue, Aurora, CO 80045, USA; Tel Aviv University, Department of Molecular Microbiology and Biotechnology, Haim Levanon Street, Tel Aviv 6997801, Israel. Electronic address: kobisimpsonlavy@gmail.com.
Alex BronsteinTel Aviv University, Department of Molecular Microbiology and Biotechnology, Haim Levanon Street, Tel Aviv 6997801, Israel.
Martin KupiecTel Aviv University, Department of Molecular Microbiology and Biotechnology, Haim Levanon Street, Tel Aviv 6997801, Israel.
Mark JohnstonUniversity of Colorado School of Medicine, Department of Biochemistry and Molecular Genetics, 12801 E 17(th) Avenue, Aurora, CO 80045, USA. Electronic address: mark.johnston@ucdenver.edu.
Tel Aviv University · IL

Funding

GLUCOSE SENSING AND SIGNALLING IN YEASTR01GM032540 · NIGMS · WASHINGTON UNIVERSITY · PI JOHNSTON, HENRY MARK · 1985 to 2017
$5.7M
NIGMS NIH HHS GM32540NIGMS NIH HHS R01 GM032540
6 · The paper itself

Abstract

Yeast cells with DNA damage avoid respiration, presumably because products of oxidative metabolism can be harmful to DNA. We show that DNA damage inhibits the activity of the Snf1 (AMP-activated) protein kinase (AMPK), which activates expression of genes required for respiration. Glucose and DNA damage upregulate SUMOylation of Snf1, catalyzed by the SUMO E3 ligase Mms21, which inhibits SNF1 activity. The DNA damage checkpoint kinases Mec1/ATR and Tel1/ATM, as well as the nutrient-sensing protein kinase A (PKA), regulate Mms21 activity toward Snf1. Mec1 and Tel1 are required for two SNF1-regulated processes-glucose sensing and ADH2 gene expression-even without exogenous genotoxic stress. Our results imply that inhibition of Snf1 by SUMOylation is a mechanism by which cells lower their respiration in response to DNA damage. This raises the possibility that activation of DNA damage checkpoint mechanisms could contribute to aerobic fermentation (Warburg effect), a hallmark of cancer cells.

Indexed as

DNA DamageCyclic AMP-Dependent Protein KinasesIntracellular Signaling Peptides and ProteinsPhosphorylationProtein Serine-Threonine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSUMO-1 ProteinSumoylationCyclic AMP-Dependent Protein KinasesIntracellular Signaling Peptides and ProteinsMEC1 protein, S cerevisiaeMms21 protein, S cerevisiaeProtein Serine-Threonine KinasesSaccharomyces cerevisiae ProteinsSNF1-related protein kinasesSUMO-1 ProteinTEL1 protein, S cerevisiae

Identifiers

PMID26344768
PMCPMC4581987
OpenAlexW1779988021

What OpenQuestion holds

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Registered trials

None linked

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.