Evidence map›Paper›PMID 22670226›Full record

ArticleG3 (Bethesda, Md.)2012

Identification of Mutant Versions of the Spt16 Histone Chaperone That Are Defective for Transcription-Coupled Nucleosome Occupancy in Saccharomyces cerevisiae.

Sarah J Hainer, Brittany A Charsar, Shayna B Cohen, Joseph A Martens

Open access · goldAbstract read
In one paragraph

Article in G3 (Bethesda, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Structure and function of the histone chaperone FACT - Resolving FACTual issues.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Structure of the human histone chaperone FACT Spt16 N-terminal domain.Acta crystallographica. Section F, Structural biology communications · 2016
    Article
  17. Article
  18. Article
  19. 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.

Sarah J HainerDepartment of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15260.
Brittany A Charsar
Shayna B Cohen
Joseph A Martens
University of Pittsburgh · US

Funding

Phase I/II Partnership in Biomedical DiscoveryR25RR020463 · NCRR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JACOBSON, LEWIS A · 2006 to 2010
$1.4M
Analysis of intergenic transcription and its roles in yeast gene expressionR01GM080470 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MARTENS, JOSEPH A. · 2007 to 2011
$1.2M
NCRR NIH HHS R25 RR020463NIGMS NIH HHS R01 GM080470
6 · The paper itself

Abstract

The highly conserved FACT (Facilitates Chromatin Transactions) complex performs essential functions in eukaryotic cells through the reorganization of nucleosomes. During transcription, FACT reorganizes nucleosomes to allow passage of RNA Polymerase II and then assists in restoring these nucleosomes after RNA Polymerase II has passed. We have previously shown, consistent with this function, that Spt16 facilitates repression of the Saccharomyces cerevisiae SER3 gene by maintaining nucleosome occupancy over the promoter of this gene as a consequence of intergenic transcription of SRG1 noncoding DNA. In this study, we report the results of a genetic screen to identify mutations in SPT16 that derepress SER3. Twenty-five spt16 mutant alleles were found to derepress SER3 without causing significant reductions in either SRG1 RNA levels or Spt16 protein levels. Additional phenotypic assays indicate that these mutants have general transcription defects related to altered chromatin structure. Our analyses of a subset of these spt16 mutants reveal defects in SRG1 transcription-coupled nucleosome occupancy over the SER3 promoter. We provide evidence that these mutants broadly impair transcription-coupled nucleosome occupancy at highly transcribed genes but not at lowly transcribed genes. Finally, we show that one consequence shared by these mutations is the reduced binding of mutant Spt16 proteins across SRG1 and other highly transcribed genes. Taken together, our results highlight an important role for Spt16 in orchestrating transcription-coupled nucleosome assembly at highly transcribed regions of the genome, possibly by facilitating the association of Spt16 during this process.

Indexed as

chromatinFACTintergenic DNASpt16transcription

Identifiers

PMID22670226
PMCPMC3362939
OpenAlexW2113687453

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.