The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.
SOX9 Regulates Multiple Genes in Chondrocytes, Including Genes Encoding ECM Proteins, ECM Modification Enzymes, Receptors, and Transporters
Open accessAbstract
The transcription factor SOX9 plays an essential role in determining the fate of several cell types and is a master factor in regulation of chondrocyte development. Our aim was to determine which genes in the genome of chondrocytes are either directly or indirectly controlled by SOX9. We used RNA-Seq to identify genes whose expression levels were affected by SOX9 and used SOX9 ChIP-Seq to identify those genes that harbor SOX9-interaction sites. For RNA-Seq, the RNA expression profile of primary Sox9flox/flox mouse chondrocytes infected with Ad-CMV-Cre was compared with that of the same cells infected with a control adenovirus. Analysis of RNA-Seq data indicated that, when the levels of Sox9 mRNA were decreased more than 8-fold by infection with Ad-CMV-Cre, 196 genes showed a decrease in expression of at least 4-fold. These included many cartilage extracellular matrix (ECM) genes and a number of genes for ECM modification enzymes (transferases), membrane receptors, transporters, and others. In ChIP-Seq, 75% of the SOX9-interaction sites had a canonical inverted repeat motif within 100 bp of the top of the peak. SOX9-interaction sites were found in 55% of the genes whose expression was decreased more than 8-fold in SOX9-depleted cells and in somewhat fewer of the genes whose expression was reduced more than 4-fold, suggesting that these are direct targets of SOX9. The combination of RNA-Seq and ChIP-Seq has provided a fuller understanding of the SOX9-controlled genetic program of chondrocytes.
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“Among the upregulated genes were previously characterized SOX9 target genes, such as ECM genes encoding collagens IX and XI (53), as well as other TF genes like SOX5, SOX6, CREB3L2, and NFIA”
From SOX9 reprograms endothelial cells by altering the chromatin landscape (2022) · cites this paper as [53]
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“which are similar to previously identified motifs for SOX9 (5,17,53,62).”
From SOX9 reprograms endothelial cells by altering the chromatin landscape (2022) · cites this paper as [53]
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Cites
Comprehensive molecular characterization of human colon and rectal cancer
The Cancer Genome Atlas Network (2012) · Nature · doi:10.1038/nature11252 · Cited by 8,499
Mammalian microRNAs predominantly act to decrease target mRNA levels
Guo, H., Ingolia, N. T., Weissman, J. S., & Bartel, D. P. (2010) · Nature · doi:10.1038/nature09267 · Cited by 3,886
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“, floxed) [2] or wild-type mice and were cultured as described previously [54].”
BackgroundMethodInfluentialCampomelic dysplasia and autosomal sex reversal caused by mutations in an SRY-related gene
Foster, J. W., Dominguez-Steglich, M., Guioli, S., Kwok, C., Weller, P., Stevanović, M., Weissenbach, J., Mansour, S., Young, I., Goodfellow, P., et al. (1994) · Nature · doi:10.1038/372525a0 · Cited by 1,602 · cited 1×
“Heterozygous mutations in Sox9 cause campomelic dysplasia, a generalized and severe disease of cartilage characterized by hypoplasia of endochondral bone [3,4].”
BackgroundShiang, R., Thompson, L. M., Zhu, Y., Church, D. M., Fielder, T. J., Bocian, M. E., Winokur, S. T., & Wasmuth, J. J. (1994) · Cell · doi:10.1016/0092-8674(94)90302-6 · Cited by 1,329 · cited 1×
“Mutations in the transmembrane domain of FGFR3 cause the most common genetic form of dwarfism, achondroplasia [20], probably because FGFR3 controls the proliferation of chondrocytes and has been shown to stimulate SOX9 expression [10].”
BackgroundSOX9 Is a Potent Activator of the Chondrocyte-Specific Enhancer of the Proα1(II) Collagen Gene
Lefebvre, V., Huang, W., Harley, V. R., Goodfellow, P. N., & Crombrugghe, B. D. (1997) · Molecular and Cellular Biology · doi:10.1128/mcb.17.4.2336 · Cited by 1,077
Lefebvre, V., Li, P., & de Crombrugghe, B. (1998) · The EMBO Journal · doi:10.1093/emboj/17.19.5718 · Cited by 811 · cited 1×
“It is possible that SOX5 and SOX6 bind near SOX9-binding sites and regulate gene expression together with SOX9 [49].”
BackgroundA Stem Cell–Based Approach to Cartilage Repair
Johnson, K., Zhu, S., Tremblay, M. S., Payette, J. N., Wang, J., Bouchez, L. C., Meeusen, S., Althage, A., Cho, C. Y., Wu, X., et al. (2012) · Science · doi:10.1126/science.1215157 · Cited by 810
Interactions between Sox9 and β-catenin control chondrocyte differentiationPreprint
Akiyama, H., Lyons, J. P., Mori–Akiyama, Y., Yang, X., Zhang, R., Zhang, Z., Deng, J. M., Taketo, M. M., Nakamura, T., Behringer, R. R., et al. (2004) · Genes & Development · doi:10.1101/gad.1171104 · Cited by 755
Self-citationMaskless fabrication of light-directed oligonucleotide microarrays using a digital micromirror array
Singh‐Gasson, S., Green, R. D., Yue, Y., Nelson, C. J., Blattner, F. R., Sussman, M. R., & Cerrina, F. (1999) · Nature Biotechnology · doi:10.1038/13664 · Cited by 733 · cited 1×
“To identify all the direct targets of SOX9 in the genome of chondrocytes, we used chromatin immunoprecipitation sequencing (ChIP-Seq), a method for genome-wide profiling of DNA binding and chromatin proteins, which offers higher resolution and greater coverage than its array-based predecessor ChIP on chip array [16,17…”
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Template Switching as a Driver of Promoter Evolution in Yeast: Case Study of the GRE2 Gene
Rozenfeld, M., Bachar, M., Cohen, R., Marcos‐Hadad, E., Milo, S., Covo, S., & Hazkani‐Covo, E. (2026) · Genome Biology and Evolution · doi:10.1093/gbe/evag078
Metadata
- Authors
- Oh, C.-D., Lu, Y., Liang, S., Mori-Akiyama, Y., Chen, D., de Crombrugghe, B., & Yasuda, H.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Rush University Medical Center (US)
- Corresponding author
- Yasuda, Hideyo
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2014-09-17
- Volume
- 9
- Issue
- 9
- Pages
- e107577
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4168005
- OpenAlex
- W2040278668
- Cited by
- 101
- References
- 54
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 7 · 2023: 4 · 2022: 9 · 2021: 9 · 2020: 17 · 2019: 10 · 2018: 6 · 2017: 6 · 2016: 11 · 2015: 14
- FWCI
- 8.59
- Type
- journal article
- Language
- en
- Update notices
- correction (2015-11-12)
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- National Institutes of Health (CA-16 672)
- University of Texas MD Anderson Cancer Center (#CA16672)
- National Cancer Institute (CA-16672, P30CA016672)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR309854, R01AR054465)
- Topics
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Proteoglycans and glycosaminoglycans research
- Keywords
- SOX9, chondrocytes, transcriptional regulation, extracellular matrix genes, transcription factor binding sites, gene expression profiling, Cre-loxP conditional knockout, chondrogenesis, cell surface receptors, transporters
- MeSH terms
- Animals, Binding Sites, Gene Expression Regulation, Humans, Protein Binding, Gene Expression, Extracellular Matrix Proteins, Mice, Knockout, Chondrocytes, Gene Expression Profiling, Protein Transport, Chromatin Immunoprecipitation, Mice, SOX9 Transcription Factor, Position-Specific Scoring Matrices, High-Throughput Nucleotide Sequencing, Nucleotide Motifs
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