Evidence map›Paper›PMID 26149683›Full record

ArticleThe Journal of biological chemistry2015

Dimethylated H3K27 Is a Repressive Epigenetic Histone Mark in the Protist Entamoeba histolytica and Is Significantly Enriched in Genes Silenced via the RNAi Pathway.

Bardees M Foda, Upinder Singh

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. 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
2.9field-weighted citation impact, top 9% 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, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Biology · 2022
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Effect of periostin silencing on Runx2, RANKL and OPG expression in osteoblasts.Journal of orofacial orthopedics = Fortschritte der Kieferorthopadie : Organ/official journal Deutsche Gesellschaft fur Kieferorthopadie · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Telomeric Repeat-Binding Factor Homologs inFrontiers in cellular and infection microbiology · 2018
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Recent advances inF1000Research · 2016
    Review
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

2 authors at 1 institution in 2 countries.

Bardees M FodaDepartments of Internal Medicine, Division of Infectious Diseases, School of Medicine, Stanford University, Stanford, California 94305; Department of Molecular Genetics and Enzymology, National Research Centre, Dokki, Egypt.
Upinder SinghDepartments of Internal Medicine, Division of Infectious Diseases, School of Medicine, Stanford University, Stanford, California 94305; Departments of Microbiology and Immunology, School of Medicine, Stanford University, Stanford, California 94305. Electronic address: usingh@stanford.edu.
Stanford University · US

Funding

Investigating Entamoeba histolytica Colonic PathogenesisR01AI053724 · NIAID · STANFORD UNIVERSITY · PI SINGH, UPINDER · 2003 to 2012
$3.8M
Development of Genetic Tools in Entamoeba histolyticaR21AI102277 · NIAID · STANFORD UNIVERSITY · PI SINGH, UPINDER · 2012 to 2013
$420k
NIAID NIH HHS R01 AI053724NIAID NIH HHS R01AI053724NIAID NIH HHS R21 AI102277
6 · The paper itself

Abstract

RNA interference (RNAi) is a fundamental biological process that plays a crucial role in regulation of gene expression in many organisms. Transcriptional gene silencing (TGS) is one of the important nuclear roles of RNAi. Our previous data show that Entamoeba histolytica has a robust RNAi pathway that links to TGS via Argonaute 2-2 (Ago2-2) associated 27-nucleotide small RNAs with 5'-polyphosphate termini. Here, we report the first repressive histone mark to be identified in E. histolytica, dimethylation of H3K27 (H3K27Me2), and demonstrate that it is enriched at genes that are silenced by RNAi-mediated TGS. An RNAi-silencing trigger can induce H3K27Me2 deposits at both episomal and chromosomal loci, mediating gene silencing. Our data support two phases of RNAi-mediated TGS: an active silencing phase where the RNAi trigger is present and both H3K27Me2 and Ago2-2 concurrently enrich at chromosomal loci; and an established silencing phase in which the RNAi trigger is removed, but gene silencing with H3K27Me2 enrichment persist independently of Ago2-2 deposition. Importantly, some genes display resistance to chromosomal silencing despite induction of functional small RNAs. In those situations, the RNAi-triggering plasmid that is maintained episomally gets partially silenced and has H3K27Me2 enrichment, but the chromosomal copy displays no repressive histone enrichment. Our data are consistent with a model in which H3K27Me2 is a repressive histone modification, which is strongly associated with transcriptional repression. This is the first example of an epigenetic histone modification that functions to mediate RNAi-mediated TGS in the deep-branching eukaryote E. histolytica.

Indexed as

Gene SilencingTranscription, GeneticAmino Acid SequenceArgonaute ProteinsChromosomesDNA MethylationEntamoeba histolyticaHistonesModels, GeneticMolecular Sequence DataPlasmidsProtozoan ProteinsSequence AlignmentSignal TransductionArgonaute ProteinsHistonesProtozoan Proteinsargonautechromatin immunoprecipitation (ChiP)Entamoeba histolyticaepigeneticsgene expressionH3K27Me2histone methylationparasitologyRNA interference (RNAi)transcriptional gene silencing

Identifiers

PMID26149683
PMCPMC4543668
OpenAlexW1596140428

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.