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Impaired intervertebral disc formation in the absence of Jun

Axel Behrens1, Jody Haigh, Fatima Mechta-Grigoriou

  • 1Research Institute of Molecular Pathology, Dr Bohr-Gasse 7, A-1030 Vienna, Austria.

Development (Cambridge, England)
|November 21, 2002
PubMed

Insights

The transcription factor Jun is crucial for embryonic development and axial skeleton formation. Its absence leads to notochord cell death, abnormal intervertebral discs, and scoliosis.

Area of Science:

  • Developmental Biology
  • Genetics
  • Skeletal Biology

Background:

  • Jun is a key component of the AP-1 transcription factor, vital for embryonic development.
  • Complete absence of Jun leads to embryonic lethality by mid-gestation.

Purpose of the Study:

  • To investigate novel functions of Jun using conditional inactivation.
  • To elucidate the role of Jun in axial skeleton development.

Main Methods:

  • Utilized cre/LoxP-mediated recombination for ubiquitous mosaic inactivation of a conditional Jun allele.
  • Employed collagen2a1-cre for specific Jun deletion in the notochord and sclerotome.

Main Results:

  • Jun deficiency caused severe axial skeleton malformations.
  • Specific deletion in notochord/sclerotome led to increased notochordal cell apoptosis and hypocellular intervertebral discs.
  • Vertebral body fusion resulted in scoliosis.

Conclusions:

  • Jun is essential for axial skeletogenesis.
  • Jun regulates notochord cell survival and intervertebral disc formation, preventing vertebral defects.

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