Evidence map›Paper›PMID 22308403›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Analysis of Gal4-directed transcription activation using Tra1 mutants selectively defective for interaction with Gal4.

Ling Lin, Lynn Chamberlain, Lihua J Zhu, Michael R Green

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. 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
0.7field-weighted citation impact, top 31% 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, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The biochemical and genetic discovery of the SAGA complex.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. The Pseudokinase Domain ofG3 (Bethesda, Md.) · 2018
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Mechanisms of Mediator complex action in transcriptional activation.Cellular and molecular life sciences : CMLS · 2013
    Review
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 2 institutions in 1 country.

Ling LinHoward Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Lynn Chamberlain
Lihua J Zhu
Michael R Green
Howard Hughes Medical Institute · USUniversity of Massachusetts Chan Medical School · US

Funding

TRANSCRIPTIONAL ACTIVATION BY THE ADENOVIRUS ELA PROTEINR01GM033977 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GREEN, MICHAEL R · 1985 to 2013
$3.2M
Howard Hughes Medical InstituteNIGMS NIH HHS R01 GM033977NIGMS NIH HHS R01GM033977
6 · The paper itself

Abstract

Promoter-specific transcriptional activators (activators) stimulate transcription through direct interactions with one or more components of the transcription machinery, termed the "target." The identification of direct in vivo targets of activators has been a major challenge. Previous studies have provided evidence that the Tra1 subunit of the yeast SAGA (Spt-Ada-Gcn5-acetyltransferase) complex is the target of the yeast activator Gal4. However, several other general transcription factors, in particular the mediator complex, have also been implicated as Gal4 targets. Here we perform a large-scale genetic screen to derive and characterize tra1 alleles that are selectively defective for interaction with Gal4 in vivo [Gal4 interaction defective (GID) mutants]. In contrast to WT Tra1, Tra1 GID mutants are not recruited by Gal4 to the promoter and cannot support Gal4-directed transcription, demonstrating the essentiality of the Gal4-Tra1 interaction. In yeast strains expressing a Tra1 GID mutant, binding of Gal4 to the promoter is unexpectedly also diminished, indicating that Gal4 and Tra1 bind cooperatively. Consistent with cooperative binding, we demonstrate that the Gal4-Tra1 interaction occurs predominantly on the promoter and not off DNA. Finally, we show that although Tra1 is targeted by other activators, these interactions are unaffected by GID mutations, revealing an unanticipated specificity of the Gal4-Tra1 interaction.

Indexed as

Binding SitesBiological AssayDNA-Binding ProteinsDNA, FungalFluorescenceGalactokinaseGalactoseGene Expression Regulation, FungalHistone AcetyltransferasesMutationPromoter Regions, GeneticProtein BindingSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTrans-ActivatorsTranscriptional ActivationDNA-Binding ProteinsDNA, FungalGAL1 protein, S cerevisiaeGAL4 protein, S cerevisiaeGalactokinaseGalactoseHistone AcetyltransferasesSaccharomyces cerevisiae ProteinsTRA1 protein, S cerevisiaeTrans-ActivatorsTranscription Factors

Identifiers

PMID22308403
PMCPMC3277556
OpenAlexW2094075502

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.