ArticleScientific reports2019
Differential transactivation of the upstream aggrecan enhancer regulated by PAX1/9 depends on SOX9-driven transactivation.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
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- Getting to the Core: Exploring the Embryonic Development from Notochord to Nucleus Pulposus.Journal of developmental biology · 2024Review
- Deletion of Pax1 scoliosis-associated regulatory elements leads to a female-biased tail abnormality.Cell reports · 2024Article
- Therapeutic factors and biomaterial-based delivery tools for degenerative intervertebral disc repair.Frontiers in cell and developmental biology · 2024Review
- Recommendations for intervertebral disc notochordal cell investigation: From isolation to characterization.JOR spine · 2023Article
- PDGFRβCell reports · 2022Article
- Integrated regulation of chondrogenic differentiation in mesenchymal stem cells and differentiation of cancer cells.Cancer cell international · 2022Review
- An overview of PAX1: Expression, function and regulation in development and diseases.Frontiers in cell and developmental biology · 2022Review
- Pathomechanism of intervertebral disc degeneration.JOR spine · 2020Review
- The cartilage matrisome in adolescent idiopathic scoliosis.Bone research · 2020Review
- The Bone-Forming Properties of Periosteum-Derived Cells Differ Between Harvest Sites.Frontiers in cell and developmental biology · 2020Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A previously identified enhancer 10 kb upstream of the Aggrecan (Acan) gene (UE) can drive cartilage specific reporter expression in vivo. Here, we report that the paralogous transcription factors PAX1 and PAX9 differentially drive UE, depending on the presence or absence of SOX9-driven transactivation. In the developing vertebral column, PAX1/9 expression was inversely correlated with Acan expression. Moreover, PAX1/9 was co-expressed with SOX9/5/6 in the intervertebral mesenchyme and the inner annulus fibrosus (AF), and with SOX9 in the outer AF. Significant Acan upregulation was observed during chondrification of Pax1-silenced AF cells, while, Acan was significantly downregulated by persistent expression of Pax1 in cartilage. Deletion of UE using CRISPR/Cas9 resulted in ~30% and ~40% reduction of Acan expression in cartilage and the AF, respectively. In the UE, PAX1/9 acts as weak transactivators through a PAX1/9-binding site partially overlapped with a SOX9-binding site. In the presence of SOX9, which otherwise drives robust Acan expression along with SOX5/6, PAX1/9 competes with SOX9 for occupancy of the binding site, resulting in reduced transactivation of Acan. Coimmunoprecipitation revealed the physical interaction of Pax1 with SOX9. Thus, transactivation of the UE is differentially regulated by concerted action of PAX1/9, SOX9, and SOX5/6 in a context-dependent manner.
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