Evidence map›Paper›PMID 20502685›Full record

ArticlePLoS genetics2010

FACT prevents the accumulation of free histones evicted from transcribed chromatin and a subsequent cell cycle delay in G1.

Macarena Morillo-Huesca, Douglas Maya, Mari Cruz Muñoz-Centeno, Rakesh Kumar Singh, Vincent Oreal, Gajjalaiahvari Ugander Reddy, Dun Liang, Vincent Géli, Akash Gunjan, Sebastián Chávez

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.5field-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

41 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Extra-nuclear histones: origin, significance and perspectives.Molecular and cellular biochemistry · 2022
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Chromatin Stability as a Target for Cancer Treatment.BioEssays : news and reviews in molecular, cellular and developmental biology · 2019
    Review
  11. Article
  12. Structure and function of the histone chaperone FACT - Resolving FACTual issues.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. 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

10 authors at 2 institutions in 2 countries.

Macarena Morillo-HuescaDepartamento de Genética, Universidad de Sevilla, Seville, Spain.
Douglas Maya
Mari Cruz Muñoz-Centeno
Rakesh Kumar Singh
Vincent Oreal
Gajjalaiahvari Ugander Reddy
Dun Liang
Vincent Géli
Akash Gunjan
Sebastián Chávez
Florida State University · USUniversidad de Sevilla · ES

Funding

Regulation of histone genes upon replication arrest and DNA damage R15GM079678 · NIGMS · FLORIDA STATE UNIVERSITY · PI PAIK, HYERYUN JOHANNA · 2007 to 2007
$215k
NIGMS NIH HHS R15 GM079678NIGMS NIH HHS R15GM079678-01
6 · The paper itself

Abstract

The FACT complex participates in chromatin assembly and disassembly during transcription elongation. The yeast mutants affected in the SPT16 gene, which encodes one of the FACT subunits, alter the expression of G1 cyclins and exhibit defects in the G1/S transition. Here we show that the dysfunction of chromatin reassembly factors, like FACT or Spt6, down-regulates the expression of the gene encoding the cyclin that modulates the G1 length (CLN3) in START by specifically triggering the repression of its promoter. The G1 delay undergone by spt16 mutants is not mediated by the DNA-damage checkpoint, although the mutation of RAD53, which is otherwise involved in histone degradation, enhances the cell-cycle defects of spt16-197. We reveal how FACT dysfunction triggers an accumulation of free histones evicted from transcribed chromatin. This accumulation is enhanced in a rad53 background and leads to a delay in G1. Consistently, we show that the overexpression of histones in wild-type cells down-regulates CLN3 in START and causes a delay in G1. Our work shows that chromatin reassembly factors are essential players in controlling the free histones potentially released from transcribed chromatin and describes a new cell cycle phenomenon that allows cells to respond to excess histones before starting DNA replication.

Indexed as

Blotting, NorthernChromatinChromatin ImmunoprecipitationCyclinsDNA-Binding ProteinsDown-RegulationG1 PhaseHigh Mobility Group ProteinsHistonesPhosphorylationPromoter Regions, GeneticRNA, MessengerSaccharomyces cerevisiae ProteinsTranscriptional Elongation FactorsChromatinCLN3 protein, S cerevisiaeCyclinsDNA-Binding ProteinsFACT protein, S cerevisiaeHigh Mobility Group ProteinsHistonesRNA, MessengerSaccharomyces cerevisiae ProteinsSPT16 protein, S cerevisiaeTranscriptional Elongation Factors

Identifiers

PMID20502685
PMCPMC2873916
OpenAlexW2047156847

What OpenQuestion holds

Textmetadata
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.