ArticleMolecular and cellular biology1996
An 18-base-pair sequence in the mouse proalpha1(II) collagen gene is sufficient for expression in cartilage and binds nuclear proteins that are selectively expressed in chondrocytes.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 133 citations in OpenAlex.
- Variants in the SOX9 transactivation middle domain induce axial skeleton dysplasia and scoliosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Fgfr3 enhancer deletion markedly improves all skeletal features in a mouse model of achondroplasia.The Journal of clinical investigation · 2025Article
- Serinc5 Regulates Sequential Chondrocyte Differentiation by Inhibiting Sox9 Function in Pre-Hypertrophic Chondrocytes.Journal of cellular physiology · 2025Article
- Chromatin profiling identifies chondrocyte-specific Sox9 enhancers important for skeletal development.JCI insight · 2024Article
- Sox9 Inhibits Cochlear Hair Cell Fate by Upregulating Hey1 and HeyL Antagonists of Atoh1.Cells · 2023Article
- Chondrocyte Homeostasis and Differentiation: Transcriptional Control and Signaling in Healthy and Osteoarthritic Conditions.Life (Basel, Switzerland) · 2023Review
- Emerging RUNX2-Mediated Gene Regulatory Mechanisms Consisting of Multi-Layered Regulatory Networks in Skeletal Development.International journal of molecular sciences · 2023Review
- Cartilage-Specific Cre Recombinase Transgenes/Alleles in the Mouse.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Biochemical characteristics of the chondrocyte-enriched SNORC protein and its transcriptional regulation by SOX9.Scientific reports · 2020Article
- Histone ChIP-Seq identifies differential enhancer usage during chondrogenesis as critical for defining cell-type specificity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Insights into Gene Regulatory Networks in Chondrocytes.International journal of molecular sciences · 2019Review
- Specific, Sensitive, and Stable Reporting of Human Mesenchymal Stromal Cell Chondrogenesis.Tissue engineering. Part C, Methods · 2019Article
- SOX9 is dispensable for the initiation of epigenetic remodeling and the activation of marker genes at the onset of chondrogenesis.Development (Cambridge, England) · 2018Article
- Skeletal Characterization of the Fgfr3 Mouse Model of Achondroplasia Using Micro-CT and MRI Volumetric Imaging.Scientific reports · 2018Article
- Transcriptional Network Controlling Endochondral Ossification.Journal of bone metabolism · 2017Review
- A Novel Regulatory Mechanism of Type II Collagen Expression via a SOX9-dependent Enhancer in Intron 6.The Journal of biological chemistry · 2017Article
- Signaling Cascades Governing Cdc42-Mediated Chondrogenic Differentiation and Mensenchymal Condensation.Genetics · 2016Article
- The transcription factors SOX9 and SOX5/SOX6 cooperate genome-wide through super-enhancers to drive chondrogenesis.Nucleic acids research · 2015Article
- Distinct Transcriptional Programs Underlie Sox9 Regulation of the Mammalian Chondrocyte.Cell reports · 2015Article
- How to build an inducible cartilage-specific transgenic mouse.Arthritis research & therapy · 2014Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The molecular mechanisms by which mesenchymal cells differentiate into chondrocytes are still poorly understood. We have used the gene for a chondrocyte marker, the proalpha1(II) collagen gene (Col2a1), as a model to delineate a minimal sequence needed for chondrocyte expression and identify chondrocyte-specific proteins binding to this sequence. We previously localized a cartilage-specific enhancer to 156 bp of the mouse Col2a1 intron 1. We show here that four copies of a 48-bp subsegment strongly increased promoter activity in transiently transfected rat chondrosarcoma (RCS) cells and mouse primary chondrocytes but not in 10T1/2 fibroblasts. They also directed cartilage specificity in transgenic mouse embryos. These 48 bp include two 11-bp inverted repeats with only one mismatch. Tandem copies of an 18-bp element containing the 3' repeat strongly enhanced promoter activity in RCS cells and chondrocytes but not in fibroblasts. Transgenic mice harboring 12 copies of this 18-mer expressed luciferase in ribs and vertebrae and in isolated chondrocytes but not in noncartilaginous tissues except skin and brain. In gel retardation assays, an RCS cell-specific protein and another closely related protein expressed only in RCS cells and primary chondrocytes bound to a 10-bp sequence within the 18-mer. Mutations in these 10 bp abolished activity of the multimerized 18-bp enhancer, and deletion of these 10 bp abolished enhancer activity of 465- and 231-bp intron 1 segments. This sequence contains a low-affinity binding site for POU domain proteins, and competition experiments with a high-affinity POU domain binding site strongly suggested that the chondrocyte proteins belong to this family. Together, our results indicate that an 18-bp sequence in Col2a1 intron 1 controls chondrocyte expression and suggest that RCS cells and chondrocytes contain specific POU domain proteins involved in enhancer activity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.