Evidence map›Paper›PMID 21860024›Full record

ArticleBlood2011

Gene induction and repression during terminal erythropoiesis are mediated by distinct epigenetic changes.

Piu Wong, Shilpa M Hattangadi, Albert W Cheng, Garrett M Frampton, Richard A Young, Harvey F Lodish

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
4.3field-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

94 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Erythroid Cell Research: 3D Chromatin, Transcription Factors and Beyond.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Article
  18. Reticulocyte Maturation.Membranes · 2022
    Review
  19. Review
  20. Specificity of Nuclear Size Scaling in Frog Erythrocytes.Frontiers in cell and developmental biology · 2022
    Article

34 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Piu WongWhitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.
Shilpa M Hattangadi
Albert W Cheng
Garrett M Frampton
Richard A Young
Harvey F Lodish
Whitehead Institute for Biomedical Research · USBoston Children's Hospital · USMassachusetts Institute of Technology · US

Funding

TRANSCRIPTION FACTOR GATA-1 IN TERMINAL ERYTHROID DEVELOPMENTP01HL032262 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI ZON, LEONARD IRA · 1985 to 2021
$38.9M
Crystallography CoreP30DK072437 · NIDDK · UNIVERSITY OF UTAH · PI KAPLAN, JERRY · 2005 to 2010
$4.0M
Transcriptional Regulatory Networks Active in Terminal Erythroid DifferentiationK08DK076848 · NIDDK · DANA-FARBER CANCER INST · PI HATTANGADI, SHILPA MANOHAR · 2007 to 2011
$723k
NHLBI NIH HHS L40 HL086107NHLBI NIH HHS P01 HL032262NIDDK NIH HHS K08 DK076848NIDDK NIH HHS P30 DK072437
6 · The paper itself

Abstract

It is unclear how epigenetic changes regulate the induction of erythroid-specific genes during terminal erythropoiesis. Here we use global mRNA sequencing (mRNA-seq) and chromatin immunoprecipitation coupled to high-throughput sequencing (CHIP-seq) to investigate the changes that occur in mRNA levels, RNA polymerase II (Pol II) occupancy, and multiple posttranslational histone modifications when erythroid progenitors differentiate into late erythroblasts. Among genes induced during this developmental transition, there was an increase in the occupancy of Pol II, the activation marks H3K4me2, H3K4me3, H3K9Ac, and H4K16Ac, and the elongation methylation mark H3K79me2. In contrast, genes that were repressed during differentiation showed relative decreases in H3K79me2 levels yet had levels of Pol II binding and active histone marks similar to those in erythroid progenitors. We also found that relative changes in histone modification levels, in particular, H3K79me2 and H4K16ac, were most predictive of gene expression patterns. Our results suggest that in terminal erythropoiesis both promoter and elongation-associated marks contribute to the induction of erythroid genes, whereas gene repression is marked by changes in histone modifications mediating Pol II elongation. Our data map the epigenetic landscape of terminal erythropoiesis and suggest that control of transcription elongation regulates gene expression during terminal erythroid differentiation.

Indexed as

ErythropoiesisAcetylationAnimalsCells, CulturedChromatinChromatin ImmunoprecipitationEpigenesis, GeneticErythroblastsErythroid Precursor CellsGene Expression Regulation, DevelopmentalHigh-Throughput Nucleotide SequencingHistonesHumansMiceMice, Inbred C57BLRNA, MessengerChromatinHistonesRNA, MessengerRNA Polymerase II

Identifiers

PMID21860024
PMCPMC3204918
OpenAlexW1998267774

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.