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Culturing and Measuring Fetal and Newborn Murine Long Bones
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Long bone development requires a threshold of Hox function.

Ma Carmen González-Martín1, Moises Mallo2, Marian A Ros3

  • 1Instituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), CSIC-Universidad de Cantabria-SODERCAN., 39011 Santander, Spain.

Developmental Biology
|June 17, 2014
PubMed
Summary

The Hoxd(Del(11-13)) mouse model for synpolydactyly shows delayed bone maturation and abnormal ossification. Increased Gli3 repressor activity contributes significantly to these cartilage and bone defects.

Keywords:
ChondrogenesisGli3Hoxd genesIhhOsteogenesisShort-bones

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Area of Science:

  • Developmental Biology
  • Skeletal Biology
  • Genetics

Background:

  • Synpolydactyly is a human limb malformation.
  • The Hoxd(Del(11-13)) mouse model exhibits features of synpolydactyly, including short and syndactylous digits.

Purpose of the Study:

  • To comprehensively characterize the cartilage and bone defects in Hoxd(Del(11-13)) mutants.
  • To investigate the role of Gli3 repressor activity in the observed skeletal phenotypes.

Main Methods:

  • Detailed analysis of cartilage and bone development in Hoxd(Del(11-13)) mutants.
  • Generation and analysis of double Hoxd(Del(11-13));Gli3 homozygous mutants.

Main Results:

  • Hoxd(Del(11-13)) mutants display delayed chondrocyte maturation and abnormal ossification in metacarpals/metatarsals.
  • Reduced Ihh expression and increased Gli3 repressor form correlate with the phenotype.
  • Double mutants show rescued metatarsal phenotype but only partial rescue in metacarpals.

Conclusions:

  • Hox genes are essential for long bone maturation in a dose-dependent manner.
  • Excess Gli3 repressor activity significantly contributes to the chondrogenic defects observed in Hoxd(Del(11-13)) mutants.