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Publication : Impaired intervertebral disc formation in the absence of Jun.

First Author  Behrens A Year  2003
Journal  Development Volume  130
Issue  1 Pages  103-9
PubMed ID  12441295 Mgi Jnum  J:80022
Mgi Id  MGI:2429422 Doi  10.1242/dev.00186
Citation  Behrens A, et al. (2003) Impaired intervertebral disc formation in the absence of Jun. Development 130(1):103-9
abstractText  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.
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