ArticleDevelopmental biology2013
Sost and its paralog Sostdc1 coordinate digit number in a Gli3-dependent manner.
Article in Developmental biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Increased endothelial sclerostin caused by elevated DSCAM mediates multiple trisomy 21 phenotypes.The Journal of clinical investigation · 2024Article
- Sclerostin modulates mineralization degree and stiffness profile in the fibrocartilaginous enthesis for mechanical tissue integrity.Frontiers in cell and developmental biology · 2024Article
- Endocrine Functions of Sclerostin.Current opinion in endocrine and metabolic research · 2023Article
- Differential regulation of skeletal stem/progenitor cells in distinct skeletal compartments.Frontiers in physiology · 2023Review
- Paralogous Genes Involved in Embryonic Development: Lessons from the Eye and Other Tissues.Genes · 2022Review
- Sclerostin: From Molecule to Clinical Biomarker.International journal of molecular sciences · 2022Review
- The Role of Sclerostin in Bone Diseases.Journal of clinical medicine · 2022Review
- Review
- Characterization of sclerostin's response within white adipose tissue to an obesogenic diet at rest and in response to acute exercise in male mice.Frontiers in physiology · 2022Article
- Role of Sostdc1 in skeletal biology and cancer.Frontiers in physiology · 2022Review
- Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis.Journal of clinical medicine · 2021Review
- Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin.Nature communications · 2021Article
- Endocrine role of bone in the regulation of energy metabolism.Bone research · 2021Review
- Sclerostin: from bench to bedside.Journal of bone and mineral metabolism · 2021Review
- Osteoporosis Treatment with Anti-Sclerostin Antibodies-Mechanisms of Action and Clinical Application.Journal of clinical medicine · 2021Review
- Niches for Skeletal Stem Cells of Mesenchymal Origin.Frontiers in cell and developmental biology · 2020Review
- Sostdc1 is expressed in all major compartments of developing and adult mammalian eyes.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2019Article
- Article
- Wnt Antagonists in Hematopoietic and Immune Cell Fate: Implications for Osteoporosis Therapies.Current osteoporosis reports · 2019Review
- A novel nonosteocytic regulatory mechanism of bone modeling.PLoS biology · 2019Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
WNT signaling is critical in most aspects of skeletal development and homeostasis, and antagonists of WNT signaling are emerging as key regulatory proteins with great promise as therapeutic agents for bone disorders. Here we show that Sost and its paralog Sostdc1 emerged through ancestral genome duplication and their expression patterns have diverged to delineate non-overlapping domains in most organ systems including musculoskeletal, cardiovascular, nervous, digestive, reproductive and respiratory. In the developing limb, Sost and Sostdc1 display dynamic expression patterns with Sost being restricted to the distal ectoderm and Sostdc1 to the proximal ectoderm and the mesenchyme. While Sostdc1(-/-) mice lack any obvious limb or skeletal defects, Sost(-/-) mice recapitulate the hand defects described for Sclerosteosis patients. However, elevated WNT signaling in Sost(-/-); Sostdc1(-/-) mice causes misregulation of SHH signaling, ectopic activation of Sox9 in the digit 1 field and preaxial polydactyly in a Gli1- and Gli3-dependent manner. In addition, we show that the syndactyly documented in Sclerosteosis is present in both Sost(-/-) and Sost(-/-); Sostdc1(-/-) mice, and is driven by misregulation of Fgf8 in the AER, a region lacking Sost and Sostdc1 expression. This study highlights the complexity of WNT signaling in skeletal biology and disease and emphasizes how redundant mechanism and non-cell autonomous effects can synergize to unveil new intricate phenotypes caused by elevated WNT signaling.
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Registered trials
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.