Evidence map›Paper›PMID 23754951›Full record

ArticlePLoS genetics2013

Histone acetyl transferase 1 is essential for mammalian development, genome stability, and the processing of newly synthesized histones H3 and H4.

Prabakaran Nagarajan, Zhongqi Ge, Bianca Sirbu, Cheryl Doughty, Paula A Agudelo Garcia, Michaela Schlederer, Anthony T Annunziato, David Cortez, Lukas Kenner, Mark R Parthun

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

66 citing papers in PubMed, 122 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. HAT1 Regulates Intestinal Stem Cell Proliferation and Differentiation.bioRxiv : the preprint server for biology · 2026
    Article
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  10. Review
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  15. Article
  16. Acetyltransferase in cardiovascular disease and aging.The journal of cardiovascular aging · 2024
    Article
  17. Article
  18. Article
  19. Article
  20. Article

6 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

10 authors at 5 institutions in 2 countries.

Prabakaran NagarajanDepartment of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, OH, USA.
Zhongqi Ge
Bianca Sirbu
Cheryl Doughty
Paula A Agudelo Garcia
Michaela Schlederer
Anthony T Annunziato
David Cortez
Lukas Kenner
Mark R Parthun
The Ohio State University · USBoston College · USVanderbilt University · USLudwig Boltzmann Institute for Cancer Research · ATMedical University of Vienna · AT

Funding

Structural Biology Facility CoreP30ES000267 · NIEHS · VANDERBILT UNIVERSITY · PI GUENGERICH, F PETER · 1985 to 2014
$20.3M
TRAINING PROGRAM IN ENVIRONMENTAL TOXICOLOGYT32ES007028 · NIEHS · VANDERBILT UNIVERSITY · PI F PETER Guengerich, Fiona Edith Harrison · 1985 to 2026
$15.7M
Type B Histone Acetyltransferases and the Assembly of Chromatin StructureR01GM062970 · NIGMS · OHIO STATE UNIVERSITY · PI PARTHUN, MARK R · 2001 to 2018
$5.1M
Functional Analysis of Replication Stress Response ProteinsR01CA136933 · NCI · VANDERBILT UNIVERSITY · PI CORTEZ, DAVID K · 2009 to 2013
$1.6M
NCI NIH HHS CA136933NCI NIH HHS R01 CA136933NIEHS NIH HHS P30 ES000267NIEHS NIH HHS T32 ES007028NIGMS NIH HHS GM62970NIGMS NIH HHS R01 GM062970
6 · The paper itself

Abstract

Histone acetyltransferase 1 is an evolutionarily conserved type B histone acetyltransferase that is thought to be responsible for the diacetylation of newly synthesized histone H4 on lysines 5 and 12 during chromatin assembly. To understand the function of this enzyme in a complex organism, we have constructed a conditional mouse knockout model of Hat1. Murine Hat1 is essential for viability, as homozygous deletion of Hat1 results in neonatal lethality. The lungs of embryos and pups genetically deficient in Hat1 were much less mature upon histological evaluation. The neonatal lethality is due to severe defects in lung development that result in less aeration and respiratory distress. Many of the Hat1(-/-) neonates also display significant craniofacial defects with abnormalities in the bones of the skull and jaw. Hat1(-/-) mouse embryonic fibroblasts (MEFs) are defective in cell proliferation and are sensitive to DNA damaging agents. In addition, the Hat1(-/-) MEFs display a marked increase in genome instability. Analysis of histone dynamics at sites of replication-coupled chromatin assembly demonstrates that Hat1 is not only responsible for the acetylation of newly synthesized histone H4 but is also required to maintain the acetylation of histone H3 on lysines 9, 18, and 27 during replication-coupled chromatin assembly.

Indexed as

Genomic InstabilityAcetylationAnimalsCell ProliferationCell SurvivalChromatin Assembly and DisassemblyDNA ReplicationEmbryonic DevelopmentFibroblastsHistone AcetyltransferasesHistonesHumansJumonji Domain-Containing Histone DemethylasesMiceMice, KnockoutHistone Acetyltransferaseshistone acetyltransferase type B complexHistonesJumonji Domain-Containing Histone DemethylasesKdm6b protein, mouse

Identifiers

PMID23754951
PMCPMC3675013
OpenAlexW1999477960

What OpenQuestion holds

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LicenceCC BY
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.