Evidence map›Paper›PMID 24167250›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Odd-skipped related-1 controls neural crest chondrogenesis during tongue development.

Han Liu, Yu Lan, Jingyue Xu, Ching-Fang Chang, Samantha A Brugmann, Rulang Jiang

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  6. Biomedicines · 2022
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  7. Article
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  9. Frontiers in physiology · 2022
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  15. Mkx-Deficient Mice Exhibit Hedgehog Signaling-Dependent Ectopic Ossification in the Achilles Tendons.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
    Article
  16. Article
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  19. Article
  20. Review
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

6 authors at 2 institutions in 1 country.

Han LiuDivisions of Developmental Biology and Plastic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229.
Yu Lan
Jingyue Xu
Ching-Fang Chang
Samantha A Brugmann
Rulang Jiang
Cincinnati Children's Hospital Medical Center · USNeuroDevelopment Center · US

Funding

MOLECULAR GENETIC ANALYSIS OF CRANIOFACIAL DEVELOPMENTR01DE013681 · NIDCR · UNIVERSITY OF ROCHESTER · PI JIANG, RULANG · 2000 to 2014
$6.3M
GENETIC BASIS OF CLEFT LIP AND PALATER01DE015207 · NIDCR · UNIVERSITY OF ROCHESTER · PI JIANG, RULANG · 2003 to 2012
$3.6M
NIDCR NIH HHS R01 DE013681NIDCR NIH HHS R01DE013681NIDCR NIH HHS R01 DE015207
6 · The paper itself

Abstract

The tongue is a critical element of the feeding system in tetrapod animals for their successful adaptation to terrestrial life. Whereas the oral part of the mammalian tongue contains soft tissues only, the avian tongue has an internal skeleton extending to the anterior tip. The mechanisms underlying the evolutionary divergence in tongue skeleton formation are completely unknown. We show here that the odd-skipped related-1 (Osr1) transcription factor is expressed throughout the neural crest-derived tongue mesenchyme in mouse, but not in chick, embryos during early tongue morphogenesis. Neural crest-specific inactivation of Osr1 resulted in formation of an ectopic cartilage in the mouse tongue, reminiscent in shape and developmental ontogeny of the anterior tongue cartilage in chick. SRY-box containing gene-9 (Sox9), the master regulator of chondrogenesis, is widely expressed in the nascent tongue mesenchyme at the onset of tongue morphogenesis but its expression is dramatically down-regulated concomitant with activation of Osr1 expression in the developing mouse tongue. In Osr1 mutant mouse embryos, expression of Sox9 persisted in the developing tongue mesenchyme where chondrogenesis is subsequently activated to form the ectopic cartilage. Furthermore, we show that Osr1 binds to the Sox9 gene promoter and that overexpression of Osr1 suppressed expression of endogenous Sox9 mRNAs and Sox9 promoter-driven reporter. These data indicate that Osr1 normally prevents chondrogenesis in the mammalian tongue through repression of Sox9 expression and suggest that changes in regulation of Osr1 expression in the neural crest-derived tongue mesenchyme underlie the evolutionary divergence of birds from other vertebrates in tongue morphogenesis.

Indexed as

Biological EvolutionAnimalsbeta-GalactosidaseChick EmbryoChondrogenesisGalactosidesGene Expression Regulation, DevelopmentalIndolesIn Situ HybridizationLuciferasesMiceMice, TransgenicNeural CrestReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionSequence Analysis, RNA5-bromo-4-chloro-3-indolyl beta-galactosidebeta-GalactosidaseGalactosidesIndolesLuciferasesOsr1 protein, mouseSox9 protein, mouseSOX9 Transcription FactorTranscription Factorscell fatecraniofacialdifferentiationtongue-tie

Identifiers

PMID24167250
PMCPMC3831959
OpenAlexW2069638339

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.