v-Jun downregulates the alpha 2 (I) collagen target gene indirectly through Sp1/3
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Updated: Aug 19, 2026

Laser Capture Microdissection of Mouse Embryonic Cartilage and Bone for Gene Expression Analysis
Published on: December 18, 2019
Sandrine Chamboredon1, Marc Castellazzi
1Unité de Virologie Humaine, INSERM-U412, Ecole Normale Supérieure, IFR128 BioSciences Lyon-Gerland, 46 allée d'Italie, 69364 Lyon Cedex 07, France.
Abstract:
Transformation of chick embryo fibroblasts (CEFs) by the v-Jun oncoprotein correlates with a downregulation of the alpha 2 (I) collagen gene. To investigate whether this gene constitutes a direct target of v-Jun, an analysis of a large proximal fragment of the promoter, extending from position -1080 to +109, was performed. Transient transfections with -1080/+109 and deleted derivatives revealed that a short proximal fragment, -433/+11, is the target for repression by v-Jun. Extensive analysis, conducted in CEFs and in Sp1/3-deficient Drosophila SL2 cells, further showed that (i) high constitutive activity of -433/+11 requires a direct binding of the ubiquitous Sp1 and/or Sp3 transcription factors acting on two distinct motifs, that is, a proximal TCC-rich region and an upstream GC box, and that (ii) repression by v-Jun does not require any direct binding of the oncoprotein to the DNA, but an indirect binding within a v-Jun-Sp1/3-DNA chromatin-associated complex. This situation is reminiscent of a situation previously reported with the tata-less, SPARC (secreted protein, acidic, and rich in cysteine) target promoter that regulates the expression of another extracellular matrix component in the same model of cell transformation. Taken together, these data reinforce the view that, at least in CEFs, v-Jun downregulates a family of direct target genes by binding to the DNA indirectly through Sp1/3.
Insights
The v-Jun oncoprotein downregulates the alpha 2 (I) collagen gene by indirectly binding to DNA via Sp1/3 transcription factors. This mechanism affects extracellular matrix gene expression during cell transformation.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- v-Jun oncoprotein induces transformation in chick embryo fibroblasts (CEFs).
- Transformation correlates with decreased alpha 2 (I) collagen gene expression.
- The alpha 2 (I) collagen gene is crucial for extracellular matrix formation.
Purpose of the Study:
- To determine if the alpha 2 (I) collagen gene is a direct target of v-Jun.
- To elucidate the mechanism of v-Jun-mediated gene repression.
- To investigate the role of Sp1/3 transcription factors in this process.
Main Methods:
- Analysis of the alpha 2 (I) collagen promoter using transient transfections and deletion constructs.
- Experiments conducted in chick embryo fibroblasts (CEFs) and Drosophila SL2 cells.
- Chromatin immunoprecipitation assays to study protein-DNA interactions.
Main Results:
- A proximal promoter fragment (-433/+11) was identified as the target for v-Jun repression.
- High promoter activity depends on Sp1/3 binding to GC-rich motifs.
- v-Jun represses the promoter indirectly by interacting with Sp1/3 within a DNA-bound complex.
Conclusions:
- v-Jun downregulates the alpha 2 (I) collagen gene indirectly through Sp1/3 transcription factors.
- This indirect binding mechanism is conserved in other extracellular matrix genes, like SPARC.
- v-Jun may regulate a family of direct target genes via Sp1/3 in CEFs.
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