Evidence map›Paper›PMID 23028370›Full record

ArticlePLoS genetics2012

UTX and UTY demonstrate histone demethylase-independent function in mouse embryonic development.

Karl B Shpargel, Toru Sengoku, Shigeyuki Yokoyama, Terry Magnuson

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers.

0numbers the graph read from it
0cells of the map it votes in
219citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

219 citing papers in PubMed, 313 citations in OpenAlex.

  1. Article
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  6. A RUNX2 reporter is expressed prior to osteochondral differentiation and models metaphyseal dysplasia with maxillary hypoplasia and brachydactyly.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026
    Article
  7. Review
  8. Article
  9. Article
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  11. Review
  12. Review
  13. Histone Demethylase UTX Suppresses Tumor Cell Proliferation by Regulating Stress Granules.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. UTX (KDM6A) promotes differentiation noncatalytically in somatic self-renewing epithelia.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  19. Review
  20. Article

159 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

4 authors at 2 institutions in 2 countries.

Karl B ShpargelDepartment of Genetics, Carolina Center for Genome Sciences, and Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Toru Sengoku
Shigeyuki Yokoyama
Terry Magnuson
Systems Biology Institute · JPUniversity of North Carolina at Chapel Hill · US

Funding

CENTER TO CHARACTERIZE &MAINTAIN MUTANT MICEU42RR014817 · NCRR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAGNUSON, TERRY R · 1999 to 2011
$14.9M
Albino Deletion Complex and Early Mouse DevelopmentR01GM101974 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAGNUSON, TERRY R · 2012 to 2024
$5.2M
Roles of Histone H3K27 demethylases in germ cell epigenetic developmentF32GM087905 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SHPARGEL, KARL BRYAN · 2009 to 2010
$102k
NCRR NIH HHS RR014817NCRR NIH HHS U42 RR014817NIGMS NIH HHS F32 GM087905NIGMS NIH HHS GM087905NIGMS NIH HHS NIH GM101974NIGMS NIH HHS R01 GM101974
6 · The paper itself

Abstract

UTX (KDM6A) and UTY are homologous X and Y chromosome members of the Histone H3 Lysine 27 (H3K27) demethylase gene family. UTX can demethylate H3K27; however, in vitro assays suggest that human UTY has lost enzymatic activity due to sequence divergence. We produced mouse mutations in both Utx and Uty. Homozygous Utx mutant female embryos are mid-gestational lethal with defects in neural tube, yolk sac, and cardiac development. We demonstrate that mouse UTY is devoid of in vivo demethylase activity, so hemizygous X(Utx-) Y(+) mutant male embryos should phenocopy homozygous X(Utx-) X(Utx-) females. However, X(Utx-) Y(+) mutant male embryos develop to term; although runted, approximately 25% survive postnatally reaching adulthood. Hemizygous X(+) Y(Uty-) mutant males are viable. In contrast, compound hemizygous X(Utx-) Y(Uty-) males phenocopy homozygous X(Utx-) X(Utx-) females. Therefore, despite divergence of UTX and UTY in catalyzing H3K27 demethylation, they maintain functional redundancy during embryonic development. Our data suggest that UTX and UTY are able to regulate gene activity through demethylase independent mechanisms. We conclude that UTX H3K27 demethylation is non-essential for embryonic viability.

Indexed as

Gene Expression Regulation, DevelopmentalHistone DemethylasesProteinsAnimalsEmbryonic DevelopmentFemaleHemizygoteHomozygoteHumansJumonji Domain-Containing Histone DemethylasesMaleMethylationMiceMinor Histocompatibility AntigensMutationHistone DemethylasesJumonji Domain-Containing Histone DemethylasesKdm6b protein, mouseMinor Histocompatibility AntigensProteinsUtx protein, mouseUty protein, mouse

Identifiers

PMID23028370
PMCPMC3459986
OpenAlexW2022300004

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.