Evidence map›Paper›PMID 33707608›Full record

ArticleCommunications biology2021

Dmrt2 promotes transition of endochondral bone formation by linking Sox9 and Runx2.

Koichiro Ono, Kenji Hata, Eriko Nakamura, Shota Ishihara, Sachi Kobayashi, Masako Nakanishi, Michiko Yoshida, Yoshifumi Takahata, Tomohiko Murakami, Seiichi Takenoshita and 3 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Dmrt2 regulates sex-biased neuronal development in the cingulate cortex.Cellular and molecular life sciences : CMLS · 2025
    Article
  3. Article
  4. Article
  5. The role of semaphorin 3A on chondrogenic differentiation.In vitro cellular & developmental biology. Animal · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Whole Aspect of Runx2 Functions in Skeletal Development.International journal of molecular sciences · 2022
    Review
  13. Article
  14. 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

13 authors at 5 institutions in 1 country.

Koichiro OnoDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.ORCID 0000-0002-0573-1481
Kenji HataDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan. hata@dent.osaka-u.ac.jp.ORCID 0000-0003-4367-9343
Eriko NakamuraDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Shota IshiharaDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Sachi KobayashiDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Masako NakanishiDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Michiko YoshidaDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Yoshifumi TakahataDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Tomohiko MurakamiDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.ORCID 0000-0002-5021-5494
Seiichi TakenoshitaAdvanced Clinical Research Center, Fukushima Medical University, Fukushima, Japan.
Toshihisa KomoriDepartment of Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Riko NishimuraDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan. rikonisi@dent.osaka-u.ac.jp.ORCID 0000-0001-7279-8363
Toshiyuki YonedaDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
The University of Osaka · JPFukushima Medical University · JPNagasaki University · JPNippon Medical School · JPWakayama Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endochondral bone formation is fundamental for skeletal development. During this process, chondrocytes undergo multiple steps of differentiation and coordinated transition from a proliferating to a hypertrophic stage, which is critical to advance skeletal development. Here, we identified the transcription factor Dmrt2 (double-sex and mab-3 related transcription factor 2) as a Sox9-inducible gene that promotes chondrocyte hypertrophy in pre-hypertrophic chondrocytes. Epigenetic analysis further demonstrated that Sox9 regulates Dmrt2 expression through an active enhancer located 18 kb upstream of the Dmrt2 gene and that this enhancer's chromatin status is progressively activated through chondrocyte differentiation. Dmrt2-knockout mice exhibited a dwarf phenotype with delayed initiation of chondrocyte hypertrophy. Dmrt2 augmented hypertrophic chondrocyte gene expression including Ihh through physical and functional interaction with Runx2. Furthermore, Dmrt2 deficiency reduced Runx2-dependent Ihh expression. Our findings suggest that Dmrt2 is critical for sequential chondrocyte differentiation during endochondral bone formation and coordinates the transcriptional network between Sox9 and Runx2.

Indexed as

OsteogenesisAnimalsBone and BonesCell Line, TumorChondrocytesChondrogenesisCore Binding Factor Alpha 1 SubunitDisease Models, AnimalDNA-Binding ProteinsDwarfismEpigenesis, GeneticHedgehog ProteinsHypertrophyMiceMice, Inbred C57BLMice, KnockoutCore Binding Factor Alpha 1 SubunitDmrt2 protein, mouseDNA-Binding ProteinsHedgehog Proteinsihh protein, mouseRunx2 protein, mouseSox9 protein, mouseSOX9 Transcription FactorTranscription Factors

Identifiers

PMID33707608
PMCPMC7952723
OpenAlexW3134059690

What OpenQuestion holds

Textmetadata
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.