Evidence map›Paper›PMID 22223663›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Compensatory functions of histone deacetylase 1 (HDAC1) and HDAC2 regulate transcription and apoptosis during mouse oocyte development.

Pengpeng Ma, Hua Pan, Rusty L Montgomery, Eric N Olson, Richard M Schultz

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

84 citing papers in PubMed, 144 citations in OpenAlex.

  1. Molecular mechanisms of folliculogenesis and oogenesis.Systems biology in reproductive medicine · 2026
    Review
  2. Review
  3. Versatile SMAD2 and SMAD3 epitope-tagged mouse models for genomic profiling of TGFβ signaling: Uncovering GDF9-SMAD2/3 targets.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Epigenetic Regulation of EMP/EMT-Dependent Fibrosis.International journal of molecular sciences · 2024
    Review
  15. Article
  16. Pathomechanisms of Prenatally Programmed Adult Diseases.Antioxidants (Basel, Switzerland) · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Article

24 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

5 authors at 2 institutions in 1 country.

Pengpeng MaDepartment of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Hua Pan
Rusty L Montgomery
Eric N Olson
Richard M Schultz
University of Pennsylvania · USThe University of Texas Southwestern Medical Center · US

Funding

PROTEIN PHOSPHORYLATION IN PREIMPLANTATION DEVELOPMENTR01HD022681 · NICHD · UNIVERSITY OF PENNSYLVANIA · PI SCHULTZ, RICHARD MORRIS · 1987 to 2017
$3.6M
GENE EXPRESSION IN THE PREIMPLANTATION EMBRYOR37HD022681 · NICHD · UNIVERSITY OF PENNSYLVANIA · PI SCHULTZ, RICHARD M · 1997 to 2006
$2.2M
NICHD NIH HHS HD022681NICHD NIH HHS R01 HD022681NICHD NIH HHS R37 HD022681
6 · The paper itself

Abstract

Dramatic changes in chromatin structure and histone modification occur during oocyte growth, as well as a global cessation of transcription. The role of histone modifications in these processes is poorly understood. We report the effect of conditionally deleting Hdac1 and Hdac2 on oocyte development. Deleting either gene has little or no effect on oocyte development, whereas deleting both genes results in follicle development arrest at the secondary follicle stage. This developmental arrest is accompanied by substantial perturbation of the transcriptome and a global reduction in transcription even though histone acetylation is markedly increased. There is no apparent change in histone repressive marks, but there is a pronounced decrease in histone H3K4 methylation, an activating mark. The decrease in H3K4 methylation is likely a result of increased expression of Kdm5b because RNAi-mediated targeting of Kdm5b in double-mutant oocytes results in an increase in H3K4 methylation. An increase in TRP53 acetylation also occurs in mutant oocytes and may contribute to the observed increased incidence of apoptosis. Taken together, these results suggest seminal roles of acetylation of histone and nonhistone proteins in oocyte development.

Indexed as

Transcription, GeneticAcetylationAnimalsApoptosisDNA-Binding ProteinsFemaleGene DeletionGene Expression Regulation, DevelopmentalGene TargetingHistone Deacetylase 1Histone Deacetylase 2HistonesHydroxamic AcidsInfertility, FemaleJumonji Domain-Containing Histone DemethylasesLysineDNA-Binding ProteinsHdac1 protein, mouseHdac2 protein, mouseHistone Deacetylase 1Histone Deacetylase 2HistonesHydroxamic AcidsJumonji Domain-Containing Histone DemethylasesKdm5b protein, mouseLysineRNA, Messengertrichostatin ATumor Suppressor Protein p53

Identifiers

PMID22223663
PMCPMC3286984
OpenAlexW2022018162

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.