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Impaired intervertebral disc formation in the absence of Jun

(2003) DEVELOPMENT. 130(1). p.103-109
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Abstract
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.
Keywords
Jun, notochord, skeleton, cre/loxP, mouse, C-JUN, AXIAL SKELETON, TERMINAL PHOSPHORYLATION, EMBRYONIC LETHALITY, MOUSE DEVELOPMENT, NOTOCHORD, SOMITOGENESIS, GENE, TRANSFORMATION, PROLIFERATION

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Chicago
Behrens, Axel, Jody Haigh, Fatima Mechta-Grigoriou, Andras Nagy, Moshe Yaniv, and Erwin F Wagner. 2003. “Impaired Intervertebral Disc Formation in the Absence of Jun.” Development 130 (1): 103–109.
APA
Behrens, A., Haigh, J., Mechta-Grigoriou, F., Nagy, A., Yaniv, M., & Wagner, E. F. (2003). Impaired intervertebral disc formation in the absence of Jun. DEVELOPMENT, 130(1), 103–109.
Vancouver
1.
Behrens A, Haigh J, Mechta-Grigoriou F, Nagy A, Yaniv M, Wagner EF. Impaired intervertebral disc formation in the absence of Jun. DEVELOPMENT. 2003;130(1):103–9.
MLA
Behrens, Axel, Jody Haigh, Fatima Mechta-Grigoriou, et al. “Impaired Intervertebral Disc Formation in the Absence of Jun.” DEVELOPMENT 130.1 (2003): 103–109. Print.
@article{1202141,
  abstract     = {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.},
  author       = {Behrens, Axel and Haigh, Jody and Mechta-Grigoriou, Fatima and Nagy, Andras and Yaniv, Moshe and Wagner, Erwin F},
  issn         = {0950-1991},
  journal      = {DEVELOPMENT},
  keyword      = {Jun,notochord,skeleton,cre/loxP,mouse,C-JUN,AXIAL SKELETON,TERMINAL PHOSPHORYLATION,EMBRYONIC LETHALITY,MOUSE DEVELOPMENT,NOTOCHORD,SOMITOGENESIS,GENE,TRANSFORMATION,PROLIFERATION},
  language     = {eng},
  number       = {1},
  pages        = {103--109},
  title        = {Impaired intervertebral disc formation in the absence of Jun},
  url          = {http://dx.doi.org/10.1242/dev.00186},
  volume       = {130},
  year         = {2003},
}

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