ArticleDevelopment (Cambridge, England)2024
Apical expansion of calvarial osteoblasts and suture patency is dependent on fibronectin cues.
Article in Development (Cambridge, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Evaluation of ToF-SIMS imaging for semi-quantitative mapping of BODIPY-labeled fibronectin surface gradients.The Analyst · 2026Article
- Mitochondrial transfer in the HSC-HCC-macrophage network shapes hepatocellular carcinoma progression.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Self-propagating wave drives morphogenesis of skull bones in vivo.Nature communications · 2025Article
- Lamellipodia-Mediated Osteoblast Haptotaxis Guided by Fibronectin Ligand Concentrations on a Multiplex Chip.Small (Weinheim an der Bergstrasse, Germany) · 2024Article
- Mesenchymal Wnts are required for morphogenetic movements of calvarial osteoblasts during apical expansion.Development (Cambridge, England) · 2024Article
- A novel perspective of calvarial development: the cranial morphogenesis and differentiation regulated by dura mater.Frontiers in cell and developmental biology · 2024Review
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
The skull roof, or calvaria, is comprised of interlocking plates of bones that encase the brain. Separating these bones are fibrous sutures that permit growth. Currently, we do not understand the instructions for directional growth of the calvaria, a process which is error-prone and can lead to skeletal deficiencies or premature suture fusion (craniosynostosis, CS). Here, we identify graded expression of fibronectin (FN1) in the mouse embryonic cranial mesenchyme (CM) that precedes the apical expansion of calvaria. Conditional deletion of Fn1 or Wasl leads to diminished frontal bone expansion by altering cell shape and focal actin enrichment, respectively, suggesting defective migration of calvarial progenitors. Interestingly, Fn1 mutants have premature fusion of coronal sutures. Consistently, syndromic forms of CS in humans exhibit dysregulated FN1 expression, and we also find FN1 expression altered in a mouse CS model of Apert syndrome. These data support a model of FN1 as a directional substrate for calvarial osteoblast migration that may be a common mechanism underlying many cranial disorders of disparate genetic etiologies.
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