ArticleNucleic acids research2010
The dimerization domain of SOX9 is required for transcription activation of a chondrocyte-specific chromatin DNA template.
Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- SOX9: dosage- and context-dependent functions in pancreatic development and β-cell biology.Cell communication and signaling : CCS · 2026Review
- Distinct SOX9 single-molecule dynamics characterize adult differentiation and fetal-like reprogrammed states in intestinal organoids.Stem cell reports · 2026Article
- Hypomorphic and dominant-negative impact of truncated SOX9 dysregulates Hedgehog-Wnt signaling, causing campomelia.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Flavin Adenine Dinucleotide (FAD) and Pyridoxal 5'-Phosphate (PLP) Bind to Sox9 and Alter the Expression of Key Pancreatic Progenitor Transcription Factors.International journal of molecular sciences · 2022Article
- SOX9 in organogenesis: shared and unique transcriptional functions.Cellular and molecular life sciences : CMLS · 2022Review
- SOX9 reprograms endothelial cells by altering the chromatin landscape.Nucleic acids research · 2022Article
- Pioneer factors in development and cancer.iScience · 2021Review
- Both microRNA-455-5p and -3p repress hypoxia-inducible factor-2α expression and coordinately regulate cartilage homeostasis.Nature communications · 2021Article
- SOX9: Advances in Gynecological Malignancies.Frontiers in oncology · 2021Review
- Post-translational modification of SOX family proteins: Key biochemical targets in cancer?Seminars in cancer biology · 2020Review
- SOX9: The master regulator of cell fate in breast cancer.Biochemical pharmacology · 2020Review
- SOX9 has distinct regulatory roles in alternative splicing and transcription.Nucleic acids research · 2018Article
- SOX9 is dispensable for the initiation of epigenetic remodeling and the activation of marker genes at the onset of chondrogenesis.Development (Cambridge, England) · 2018Article
- Differential tissue specific, temporal and spatial expression patterns of the Aggrecan gene is modulated by independent enhancer elements.Scientific reports · 2018Article
- A Split-Luciferase Reporter Recognizing GFP and mCherry Tags to Facilitate Studies of Protein-Protein Interactions.International journal of molecular sciences · 2017Article
- A Novel Regulatory Mechanism of Type II Collagen Expression via a SOX9-dependent Enhancer in Intron 6.The Journal of biological chemistry · 2017Article
- SOX9 directly Regulates CTGF/CCN2 Transcription in Growth Plate Chondrocytes and in Nucleus Pulposus Cells of Intervertebral Disc.Scientific reports · 2016Article
- Dimerization and Transactivation Domains as Candidates for Functional Modulation and Diversity of Sox9.PloS one · 2016Article
- Distinct Transcriptional Programs Underlie Sox9 Regulation of the Mammalian Chondrocyte.Cell reports · 2015Article
- SOXE transcription factors form selective dimers on non-compact DNA motifs through multifaceted interactions between dimerization and high-mobility group domains.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in SOX9, a gene essential for chondrocyte differentiation cause the human disease campomelic dysplasia (CD). To understand how SOX9 activates transcription, we characterized the DNA binding and cell-free transcription ability of wild-type SOX9 and a dimerization domain SOX9 mutant. Whereas formation of monomeric mutant SOX9-DNA complex increased linearly with increasing SOX9 concentrations, formation of a wild-type SOX9-DNA dimeric complex increased more slowly suggesting a more sigmoidal-type progression. Stability of SOX9-DNA complexes, however, was unaffected by the dimerization mutation. Both wild-type and mutant SOX9 activated transcription of a naked Col2a1 DNA template. However, after nucleosomal assembly, only wild-type and not the mutant was able to remodel chromatin and activate transcription of this template. Using a cell line, in which the Col2a1 vector was stably integrated, no differences were seen in the interactions of wild-type and mutant SOX9 with the chromatin of the Col2a1 vector using ChIP. However, the mutant was unable to activate transcription in agreement with in vitro results. We hypothesize that the SOX9 dimerization domain is necessary to remodel the Col2a1 chromatin in order to allow transcription to take place. These results further clarify the mechanism that accounts for CD in patients harboring SOX9 dimerization domain mutations.
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