Evidence map›Paper›PMID 9528749›Full record

ArticleMolecular and cellular biology1998

SWI-SNF complex participation in transcriptional activation at a step subsequent to activator binding.

M P Ryan, R Jones, R H Morse

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Bcl11b/Ctip2 in Skin, Tooth, and Craniofacial System.Frontiers in cell and developmental biology · 2020
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Mechanisms of Mediator complex action in transcriptional activation.Cellular and molecular life sciences : CMLS · 2013
    Review
  10. Article
  11. Article
  12. Article
  13. A nucleosome positioned by alpha2/Mcm1 prevents Hap1 activator binding in vivo.Biochemical and biophysical research communications · 2007
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Global and specific transcriptional repression by the histone H3 amino terminus in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2003
    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

3 authors at 1 institution in 1 country.

M P RyanMolecular Genetics Program, Wadsworth Center, New York State Department of Health, and State University of New York School of Public Health, Albany 12201-2002, USA.
R Jones
R H Morse
New York State Department of Health · US

Funding

BINDING OF TRANSCRIPTION FACTORS TO CHROMATIN IN YEASTR01GM051993 · NIGMS · WADSWORTH CENTER · PI MORSE, RANDALL H · 1995 to 2002
$804k
NIGMS NIH HHS GM51993NIGMS NIH HHS R01 GM051993
6 · The paper itself

Abstract

The SWI-SNF complex in yeast and related complexes in higher eukaryotes have been implicated in assisting gene activation by overcoming the repressive effects of chromatin. We show that the ability of the transcriptional activator GAL4 to bind to a site in a positioned nucleosome is not appreciably impaired in swi mutant yeast cells. However, chromatin remodeling that depends on a transcriptional activation domain shows a considerable, although not complete, SWI-SNF dependence, suggesting that the SWI-SNF complex exerts its major effect at a step subsequent to activator binding. We tested this idea further by comparing the SWI-SNF dependence of a reporter gene based on the GAL10 promoter, which has an accessible upstream activating sequence and a nucleosomal TATA element, with that of a CYC1-lacZ reporter, which has a relatively accessible TATA element. We found that the GAL10-based reporter gene showed a much stronger SWI-SNF dependence than did the CYC1-lacZ reporter with several different activators. Remarkably, transcription of the GAL10-based reporter by a GAL4-GAL11 fusion protein showed a nearly complete requirement for the SWI-SNF complex, strongly suggesting that SWI-SNF is needed to allow access of TFIID or the RNA polymerase II holoenzyme. Taken together, our results demonstrate that chromatin remodeling in vivo can occur by both SWI-SNF-dependent and -independent avenues and suggest that the SWI-SNF complex exerts its major effect in transcriptional activation at a step subsequent to transcriptional activator-promoter recognition.

Indexed as

Gene Expression Regulation, FungalSaccharomyces cerevisiae ProteinsTranscriptional ActivationTranscription FactorsChromatinDNA-Binding ProteinsFungal ProteinsGenes, ReporterNucleosomesPromoter Regions, GeneticSaccharomyces cerevisiaeTATA BoxTrans-ActivatorsChromatinDNA-Binding ProteinsFungal ProteinsGAL4 protein, S cerevisiaeNucleosomesSaccharomyces cerevisiae ProteinsTrans-ActivatorsTranscription Factors

Identifiers

PMID9528749
PMCPMC121407
OpenAlexW2127501286

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.