Evidence map›Paper›PMID 20810924›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

A quantitative model of glucose signaling in yeast reveals an incoherent feed forward loop leading to a specific, transient pulse of transcription.

Sooraj Kuttykrishnan, Jeffrey Sabina, Laura L Langton, Mark Johnston, Michael R Brent

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Model-based transcriptome engineering promotes a fermentative transcriptional state in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. The structure of dynamic GPCR signaling networks.Wiley interdisciplinary reviews. Systems biology and medicine
    Review
  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

5 authors at 1 institution in 1 country.

Sooraj KuttykrishnanCenter for Genome Sciences and Systems Biology, Washington University, St. Louis, MO 63130, USA.
Jeffrey Sabina
Laura L Langton
Mark Johnston
Michael R Brent
Washington University in St. Louis · US

Funding

INSTITUTIONAL TRAINING GRANT IN GENOMIC SCIENCET32HG000045 · NHGRI · WASHINGTON UNIVERSITY · PI MICHAEL R BRENT, Barak A Cohen · 1997 to 2026
$8.4M
GLUCOSE SENSING AND SIGNALLING IN YEASTR01GM032540 · NIGMS · WASHINGTON UNIVERSITY · PI JOHNSTON, HENRY MARK · 1985 to 2017
$5.7M
Dissecting the wiring of yeast's glucose sensing circuitF32GM076967 · NIGMS · WASHINGTON UNIVERSITY · PI SABINA, JEFFREY · 2006 to 2008
$145k
NHGRI NIH HHS T32 HG000045NIGMS NIH HHS F32 GM076967NIGMS NIH HHS GM076967NIGMS NIH HHS GM32540NIGMS NIH HHS R01 GM032540
6 · The paper itself

Abstract

The ability to design and engineer organisms demands the ability to predict kinetic responses of novel regulatory networks built from well-characterized biological components. Surprisingly, few validated kinetic models of complex regulatory networks have been derived by combining models of the network components. A major bottleneck in producing such models is the difficulty of measuring in vivo rate constants for components of complex networks. We demonstrate that a simple, genetic approach to measuring rate constants in vivo produces an accurate kinetic model of the complex network that Saccharomyces cerevisiae employs to regulate the expression of genes encoding glucose transporters. The model predicts a transient pulse of transcription of HXT4 (but not HXT2 or HXT3) in response to addition of a small amount of glucose to cells, an outcome we observed experimentally. Our model also provides a mechanistic explanation for this result: HXT2-4 are governed by a type 2, incoherent feed forward regulatory loop involving the Rgt1 and Mig2 transcriptional repressors. The efficiency with which Rgt1 and Mig2 repress expression of each HXT gene determines which of them have a pulse of transcription in response to glucose. Finally, the model correctly predicts how lesions in the feed forward loop change the kinetics of induction of HXT4 expression.

Indexed as

Models, BiologicalDNA-Binding ProteinsGene Expression Regulation, FungalGenes, FungalGlucoseGlucose Transport Proteins, FacilitativeKineticsMetabolic Networks and PathwaysRepressor ProteinsRNA, FungalRNA, MessengerSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSignal TransductionSystems BiologyTranscription FactorsDNA-Binding ProteinsGlucoseGlucose Transport Proteins, FacilitativeHXT2 protein, S cerevisiaeHXT3 protein, S cerevisiaeHXT4 protein, S cerevisiaeMig2 protein, S cerevisiaeRepressor ProteinsRGT1 protein, S cerevisiaeRNA, FungalRNA, MessengerSaccharomyces cerevisiae ProteinsTranscription Factors

Identifiers

PMID20810924
PMCPMC2944743
OpenAlexW2011737146

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.