Evidence map›Paper›PMID 19389375›Full record

ArticleDevelopmental biology2009

Functional equivalence of the zinc finger transcription factors Osr1 and Osr2 in mouse development.

Yang Gao, Yu Lan, Catherine E Ovitt, Rulang Jiang

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.3field-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

26 citing papers in PubMed, 38 citations in OpenAlex.

  1. The making of cells and organs in xenogeneic animal bioreactor.Signal transduction and targeted therapy · 2026
    Review
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  6. Review
  7. Deficiency ofInternational journal of molecular sciences · 2023
    Article
  8. Article
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  15. A novel allele of Alx4 results in reduced Fgf10 expression and failure of eyelid fusion in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2015
    Article
  16. Review
  17. Article
  18. A glance at methods for cleft palate repair.Iranian Red Crescent medical journal · 2014
    Review
  19. The OSR1 rs12329305 polymorphism contributes to the development of congenital malformations in cases of stillborn/neonatal death.Medical science monitor : international medical journal of experimental and clinical research · 2014
    Article
  20. Odd-skipped related-1 controls neural crest chondrogenesis during tongue development.Proceedings of the National Academy of Sciences of the United States of America · 2013
    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

4 authors at 1 institution in 1 country.

Yang GaoDepartment of Biomedical Genetics and Center for Oral Biology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Yu Lan
Catherine E Ovitt
Rulang Jiang
University of Rochester · US

Funding

MOLECULAR GENETIC ANALYSIS OF CRANIOFACIAL DEVELOPMENTR01DE013681 · NIDCR · UNIVERSITY OF ROCHESTER · PI JIANG, RULANG · 2000 to 2014
$6.3M
NIDCR NIH HHS R01 DE013681NIDCR NIH HHS R01DE013681
6 · The paper itself

Abstract

Osr1 and Osr2 are the only mammalian homologs of the Drosophila odd-skipped family developmental regulators. The Osr1 protein contains three zinc-finger motifs whereas Osr2 exists in two isoforms, containing three and five zinc-finger motifs respectively, due to alternative splicing of the transcripts. Targeted null mutations in these genes in mice resulted in distinct phenotypes, with heart and urogenital developmental defects in Osr1(-/-) mice and with cleft palate and open eyelids at birth in Osr2(-/-) mice. To investigate whether these contrasting mutant phenotypes are due to differences in their protein structure or to differential expression patterns, we generated mice in which the endogenous Osr2 coding region was replaced by either Osr1 cDNA or Osr2A cDNA encoding the five-finger isoform. The knockin alleles recapitulated endogenous Osr2 mRNA expression patterns in most tissues and completely rescued cleft palate and cranial skeletal developmental defects of Osr2(-/-) mice. Mice hemizygous or homozygous for either knockin allele exhibited open-eyelids at birth, which correlated with differences in expression patterns between the knockin allele and the endogenous Osr2 gene during eyelid development. Molecular marker analyses in Osr2(-/-) and Osr2(Osr1ki/Osr1ki) mice revealed that Osr2 controls eyelid development through regulation of the Fgf10-Fgfr2 signaling pathway and that Osr1 rescued Osr2 function in maintaining Fgf10 expression during eyelid development in Osr2(Osr1ki/Osr1ki) mice. These results indicate that the distinct functions of Osr1 and Osr2 during mouse development result from evolutionary divergence of their cis regulatory sequences rather than distinct biochemical activities of their protein products.

Indexed as

AnimalsBody PatterningCell ProliferationEmbryo, MammalianEyelidsFibroblast Growth Factor 10Gene Expression Regulation, DevelopmentalMesodermMiceMice, Mutant StrainsProtein Serine-Threonine KinasesReceptor, Fibroblast Growth Factor, Type 2Signal TransductionTranscription FactorsZinc FingersFgf10 protein, mouseFgfr2 protein, mouseFibroblast Growth Factor 10Osr2 protein, mouseOXSR1 protein, mouseProtein Serine-Threonine KinasesReceptor, Fibroblast Growth Factor, Type 2Transcription Factors

Identifiers

PMID19389375
PMCPMC2690698
OpenAlexW2011179743

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Registered trials

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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.