Evidence map›Paper›PMID 24662054›Full record

ArticleMolecular and cellular biology2014

The Mi-2 homolog Mit1 actively positions nucleosomes within heterochromatin to suppress transcription.

Kevin M Creamer, Godwin Job, Sreenath Shanker, Geoffrey A Neale, Yuan-chi Lin, Blaine Bartholomew, Janet F Partridge

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. 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
1.4field-weighted citation impact, top 19% 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, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Nucleosome Positioning Regulates the Establishment, Stability, and Inheritance of Heterochromatin inProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Ten principles of heterochromatin formation and function.Nature reviews. Molecular cell biology · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  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

7 authors at 2 institutions in 1 country.

Kevin M CreamerDepartment of Biochemistry, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Godwin Job
Sreenath Shanker
Geoffrey A Neale
Yuan-chi Lin
Blaine Bartholomew
Janet F Partridge
St. Jude Children's Research Hospital · USSouthern Illinois University School of Medicine · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Chromatin Remodeling and Transcription RepressionR01GM070864 · NIGMS · SOUTHERN ILLINOIS UNIVERSITY CARBONDALE · PI BARTHOLOMEW, BLAINE · 2004 to 2012
$2.4M
Establishment of HeterochromatinR01GM084045 · NIGMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI PARTRIDGE, JANET F · 2008 to 2012
$1.8M
Chromatin Remodeling Complex in the spreading of silent heterochromatinF31AG038153 · NIA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI CREAMER, KEVIN MICHAEL · 2011 to 2013
$89k
NCI NIH HHS CCSG 2 P30 CA21765NCI NIH HHS P30 CA021765NIA NIH HHS F31 AG038153NIA NIH HHS NRSA F31-AG038153NIGMS NIH HHS NIH R01 GM070864NIGMS NIH HHS NIH R01 GM084045NIGMS NIH HHS R01 GM070864NIGMS NIH HHS R01 GM084045
6 · The paper itself

Abstract

Mit1 is the putative chromatin remodeling subunit of the fission yeast Snf2/histone deacetylase (HDAC) repressor complex (SHREC) and is known to repress transcription at regions of heterochromatin. However, how Mit1 modifies chromatin to silence transcription is largely unknown. Here we report that Mit1 mobilizes histone octamers in vitro and requires ATP hydrolysis and conserved chromatin tethering domains, including a previously unrecognized chromodomain, to remodel nucleosomes and silence transcription. Loss of Mit1 remodeling activity results in nucleosome depletion at specific DNA sequences that display low intrinsic affinity for the histone octamer, but its contribution to antagonizing RNA polymerase II (Pol II) access and transcription is not restricted to these sites. Genetic epistasis analyses demonstrate that SHREC subunits and the transcription-coupled Set2 histone methyltransferase, which is involved in suppression of cryptic transcription at actively transcribed regions, cooperate to silence heterochromatic transcripts. In addition, we have demonstrated that Mit1's remodeling activity contributes to SHREC function independently of Clr3's histone deacetylase activity on histone H3 K14. We propose that Mit1 is a chromatin remodeling factor that cooperates with the Clr3 histone deacetylase of SHREC and other chromatin modifiers to stabilize heterochromatin structure and to prevent access to the transcriptional machinery.

Indexed as

Gene Expression Regulation, FungalAmino Acid SequenceCell Cycle ProteinsChromatin Assembly and DisassemblyHeterochromatinHistone-Lysine N-MethyltransferaseHistonesMi-2 Nucleosome Remodeling and Deacetylase ComplexMolecular Sequence DataNucleosomesRepressor ProteinsRNA InterferenceRNA Polymerase IIRNA, Small InterferingSchizosaccharomycesSchizosaccharomyces pombe ProteinsCell Cycle ProteinsClr3 protein, S pombeHeterochromatinHistone-Lysine N-MethyltransferaseHistonesMi-2 Nucleosome Remodeling and Deacetylase ComplexMit1 protein, S pombeNucleosomesRepressor ProteinsRNA Polymerase IIRNA, Small InterferingSchizosaccharomyces pombe ProteinsSet2 protein, S pombe

Identifiers

PMID24662054
PMCPMC4019058
OpenAlexW2135362625

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.