Evidence map›Paper›PMID 25821983›Full record

ArticleeLife2015

The chromatin remodelers RSC and ISW1 display functional and chromatin-based promoter antagonism.

Timothy J Parnell, Alisha Schlichter, Boris G Wilson, Bradley R Cairns

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
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  5. Review
  6. Structure of the ISW1a complex bound to the dinucleosome.Nature structural & molecular biology · 2024
    Article
  7. Frontiers in epigenetics and epigenomics · 2024
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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.

Timothy J ParnellDepartment of Oncological Sciences, Howard Hughes Medical Institute, University of Utah School of Medicine, Salt Lake City, United States.
Alisha SchlichterDepartment of Oncological Sciences, Howard Hughes Medical Institute, University of Utah School of Medicine, Salt Lake City, United States.
Boris G WilsonDepartment of Oncological Sciences, Howard Hughes Medical Institute, University of Utah School of Medicine, Salt Lake City, United States.
Bradley R CairnsDepartment of Oncological Sciences, Howard Hughes Medical Institute, University of Utah School of Medicine, Salt Lake City, United States.
Howard Hughes Medical Institute · USHuntsman Cancer Institute · US

Funding

ANALYSIS OF THE CHROMATIN-REMODELING COMPLEX RSCR01GM060415 · NIGMS · UNIVERSITY OF UTAH · PI CAIRNS, BRADLEY R. · 1999 to 2011
$3.1M
Howard Hughes Medical InstituteNIGMS NIH HHS GM60415NIGMS NIH HHS R01 GM060415
6 · The paper itself

Abstract

ISWI family chromatin remodelers typically organize nucleosome arrays, while SWI/SNF family remodelers (RSC) typically disorganize and eject nucleosomes, implying an antagonism that is largely unexplored in vivo. Here, we describe two independent genetic screens for rsc suppressors that yielded mutations in the promoter-focused ISW1a complex or mutations in the 'basic patch' of histone H4 (an epitope that regulates ISWI activity), strongly supporting RSC-ISW1a antagonism in vivo. RSC and ISW1a largely co-localize, and genomic nucleosome studies using rsc isw1 mutant combinations revealed opposing functions: promoters classified with a nucleosome-deficient region (NDR) gain nucleosome occupancy in rsc mutants, but this gain is attenuated in rsc isw1 double mutants. Furthermore, promoters lacking NDRs have the highest occupancy of both remodelers, consistent with regulation by nucleosome occupancy, and decreased transcription in rsc mutants. Taken together, we provide the first genetic and genomic evidence for RSC-ISW1a antagonism and reveal different mechanisms at two different promoter architectures.

Indexed as

Chromatin Assembly and DisassemblyGene Expression Regulation, FungalAdenosine TriphosphatasesBinding, CompetitiveDNA-Binding ProteinsGene DeletionHistonesMultigene FamilyNuclear ProteinsNucleosomesPromoter Regions, GeneticProtein BindingProtein IsoformsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranscription FactorsAdenosine TriphosphatasesDNA-Binding ProteinsHistonesISW1 protein, S cerevisiaeNuclear ProteinsNucleosomesProtein IsoformsRSC complex, S cerevisiaeSaccharomyces cerevisiae ProteinsTranscription FactorschromatinchromosomesgenesISWInucleosomeremodelerRSCS. cerevisiae

Identifiers

PMID25821983
PMCPMC4423118
OpenAlexW2162996116

What OpenQuestion holds

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LicenceCC BY
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.