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doi: 10.1242/10.1242/dev.00186
1 Research Institute of Molecular Pathology (IMP), Dr Bohr-Gasse 7, A-1030
Vienna, Austria
2 Institut Pasteur, Unite des Virus Oncogenes, URA1644 du CNRS, 25, Rue du Dr
Roux, 75724 Paris Cedex 15, France
3 Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto,
Canada
* Present address: Mammalian Genetics Laboratory, Cancer Research UK, London
Research Institute, Lincoln's Inn Fields Laboratories, 44, Lincoln's Inn
Fields, London WC2A 3PX, UK
Present address: Samuel Lunenfeld Research Institute, Mount Sinai Hospital,
Toronto, Canada
Author for correspondence to (e-mail:
wagner{at}nt.imp.univie.ac.at)
Accepted 26 September 2002
Jun is a major component of the heterodimeric transcription factor AP-1 and is essential for embryonic development, as foetuses that lack Jun die at mid-gestation. Ubiquitous mosaic inactivation of a conditional Jun allele by cre/LoxP-mediated recombination was used to screen for novel functions of Jun and revealed that its absence results in severe malformations of the axial skeleton. More-specific Jun deletion by collagen2a1-cre demonstrated the essential function of Jun in the notochord and sclerotome. Mutant notochordal cells showed increased apoptosis, resulting in hypocellularity of the intervertebral discs. Subsequently, fusion of vertebral bodies caused a scoliosis of the axial skeleton. Thus, Jun is required for axial skeletogenesis by regulating notochord survival and intervertebral disc formation.
Key words: Jun, Notochord, Skeleton, cre/loxP, Mouse
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