Evidence map›Paper›PMID 36417913›Full record

ArticleMolecular cell2022

Tip60-mediated H2A.Z acetylation promotes neuronal fate specification and bivalent gene activation.

Justyna A Janas, Lichao Zhang, Jacklyn H Luu, Janos Demeter, Lingjun Meng, Samuele G Marro, Moritz Mall, Nancie A Mooney, Katie Schaukowitch, Yi Han Ng and 7 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  8. Review
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  11. Review
  12. Article
  13. Histone bivalency in CNS development.Genes & development · 2025
    Review
  14. Review
  15. BRD8 Guards the Pluripotent State by Sensing and Maintaining Histone Acetylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Structure of the human TIP60 complex.Nature communications · 2024
    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

17 authors at 2 institutions in 1 country.

Justyna A JanasDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Lichao ZhangDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Jacklyn H LuuDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Janos DemeterBaxter Laboratory, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Lingjun MengDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Samuele G MarroDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Moritz MallDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Nancie A MooneyBaxter Laboratory, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Katie SchaukowitchDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Yi Han NgDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Nan YangDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Yuhao HuangDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Gernot NeumayerDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Or GozaniDepartment of Biology, Stanford University, Stanford, CA 94305, USA.
Joshua E EliasDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Peter K JacksonDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Baxter Laboratory, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Marius WernigDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: wernig@stanford.edu.
Stanford University · USBaxter (United States) · US

Funding

Function of Protein Methylation in Chromatin and Signaling RegulationR35GM139569 · NIGMS · STANFORD UNIVERSITY · PI Or P. Gozani · 2021 to 2026
$4.0M
The role of Myt1l in the developing and adult mouse brainR01MH115999 · NIMH · STANFORD UNIVERSITY · PI SUDHOF, THOMAS C., WERNIG, MARIUS · 2019 to 2023
$3.6M
High Throughput DNA Sequencer UpgradeS10OD018220 · OD · STANFORD UNIVERSITY · PI COLLER, JOHN · 2014 to 2014
$596k
Howard Hughes Medical InstituteNIGMS NIH HHS R35 GM139569NIH HHS S10 OD018220NIMH NIH HHS R01 MH115999
6 · The paper itself

Abstract

Cell lineage specification is accomplished by a concerted action of chromatin remodeling and tissue-specific transcription factors. However, the mechanisms that induce and maintain appropriate lineage-specific gene expression remain elusive. Here, we used an unbiased proteomics approach to characterize chromatin regulators that mediate the induction of neuronal cell fate. We found that Tip60 acetyltransferase is essential to establish neuronal cell identity partly via acetylation of the histone variant H2A.Z. Despite its tight correlation with gene expression and active chromatin, loss of H2A.Z acetylation had little effect on chromatin accessibility or transcription. Instead, loss of Tip60 and acetyl-H2A.Z interfered with H3K4me3 deposition and activation of a unique subset of silent, lineage-restricted genes characterized by a bivalent chromatin configuration at their promoters. Altogether, our results illuminate the mechanisms underlying bivalent chromatin activation and reveal that H2A.Z acetylation regulates neuronal fate specification by establishing epigenetic competence for bivalent gene activation and cell lineage transition.

Indexed as

ChromatinHistonesAcetylationNucleosomesProtein Processing, Post-TranslationalTranscriptional ActivationChromatinHistonesNucleosomesAscl1bivalent chromatincell fategene activationH2A.Z acetylationH3K4me3neurogenesisreprogrammingTip60/Kat5transcription

Identifiers

PMID36417913
PMCPMC9779922
OpenAlexW4309593300

What OpenQuestion holds

Textmetadata
LicenceTDM
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.