ArticleDevelopmental biology2016
A combined series of Fgf9 and Fgf18 mutant alleles identifies unique and redundant roles in skeletal development.
Article in Developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- Fgf evolution in vertebrates: insights from cyclostomes.BMC genomics · 2026Article
- Dual-functional ROS-responsive hydrogel alleviates temporomandibular joint osteoarthritis by enhancing cartilage repair and mitigating inflammation.Materials today. Bio · 2025Article
- Roles of lncRNA in the crosstalk between osteogenesis and angiogenesis in the bone microenvironment.Journal of Zhejiang University. Science. B · 2025Review
- Single-cell profiling of penta- and tetradactyl mouse limb buds identifies mesenchymal progenitors controlling digit numbers and identities.Nature communications · 2025Article
- Impact of Different Cell Types on the Osteogenic Differentiation Process of Mesenchymal Stem Cells.Stem cells international · 2025Review
- Immunomodulation Pathogenesis and Treatment of Bone Nonunion.Orthopaedic surgery · 2024Review
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- Protective effects of ginseng and ginsenosides in the development of osteoarthritis (Review).Experimental and therapeutic medicine · 2023Review
- Loss of Fgfr1 and Fgfr2 in Scleraxis-lineage cells leads to enlarged bone eminences and attachment cell death.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- Developmental impairments of craniofacial bone and cartilage in transgenic mice expressing FGF10.Bone reports · 2023Article
- Targeted deletion of Fgf9 in tendon disrupts mineralization of the developing enthesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- EctomesenchymalFrontiers in genetics · 2023Article
- FGF9 Promotes Expression of HAS2 in Palatal Elevation via the Wnt/β-Catenin/TCF7L2 Pathway.Biomolecules · 2022Article
- NSD1 mutations deregulate transcription and DNA methylation of bivalent developmental genes in Sotos syndrome.Human molecular genetics · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Genome-wide detection of genetic structure and runs of homozygosity analysis in Anhui indigenous and Western commercial pig breeds using PorcineSNP80k data.BMC genomics · 2022Article
- Growth and mechanobiology of the tendon-bone enthesis.Seminars in cell & developmental biology · 2022Review
- The role of fibroblast growth factor 8 in cartilage development and disease.Journal of cellular and molecular medicine · 2022Review
- Roles of the fibroblast growth factor signal transduction system in tissue injury repair.Burns & trauma · 2022Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Fibroblast growth factor (FGF) signaling is a critical regulator of skeletal development. Fgf9 and Fgf18 are the only FGF ligands with identified functions in embryonic bone growth. Mice lacking Fgf9 or Fgf18 have distinct skeletal phenotypes; however, the extent of overlapping or redundant functions for these ligands and the stage-specific contributions of FGF signaling to chondrogenesis and osteogenesis are not known. To identify separate versus shared roles for FGF9 and FGF18, we generated a combined series of Fgf9 and Fgf18 null alleles. Analysis of embryos lacking alleles of Fgf9 and Fgf18 shows that both encoded ligands function redundantly to control all stages of skeletogenesis; however, they have variable potencies along the proximodistal limb axis, suggesting gradients of activity during formation of the appendicular skeleton. Congenital absence of both Fgf9 and Fgf18 results in a striking osteochondrodysplasia and revealed functions for FGF signaling in early proximal limb chondrogenesis. Additional defects were also noted in craniofacial bones, vertebrae, and ribs. Loss of alleles of Fgf9 and Fgf18 also affect the expression of genes encoding other key intrinsic skeletal regulators, including IHH, PTHLH (PTHrP), and RUNX2, revealing potential direct, indirect, and compensatory mechanisms to coordinate chondrogenesis and osteogenesis.
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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.