ArticleDevelopmental biology2018
Anti-osteogenic function of a LIM-homeodomain transcription factor LMX1B is essential to early patterning of the calvaria.
Article in Developmental biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Common and specific gene regulatory programs in zebrafish caudal fin regeneration at single-cell resolution.Genome research · 2025Article
- FGFR2 directs inhibition of WNT signaling to regulate anterior fontanelle closure during skull development.Development (Cambridge, England) · 2025Article
- Article
- The limb dorsoventral axis: Lmx1b's role in development, pathology, evolution, and regeneration.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Review
- Evolution, conservatism and overlooked homologies of the mammalian skull.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Lineage-specific mutation ofFrontiers in physiology · 2023Article
- En1 and Lmx1b do not recapitulate embryonic dorsal-ventral limb patterning functions during mouse digit tip regeneration.Cell reports · 2022Article
- LIM Homeobox Transcription Factor 1-β Expression is Upregulated in Patients with Osteolysis after Total Ankle Arthroplasty and Inhibits Receptor Activator of Nuclear Factor-κB Ligand-Induced Osteoclast Differentiation in Vitro.Journal of bone metabolism · 2022Article
- Developmentally interdependent stretcher-compressor relationship between the embryonic brain and the surrounding scalp in the preosteogenic head.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Transcription Factor Lmx1b Negatively Regulates Osteoblast Differentiation and Bone Formation.International journal of molecular sciences · 2022Article
- Making and shaping endochondral and intramembranous bones.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Review
- Dlx5-augmentation in neural crest cells reveals early development and differentiation potential of mouse apical head mesenchyme.Scientific reports · 2021Article
- What Do Animal Models Teach Us About Congenital Craniofacial Defects?Advances in experimental medicine and biology · 2020Review
- Molecular patterning of the embryonic cranial mesenchyme revealed by genome-wide transcriptional profiling.Developmental biology · 2019Article
- A tale of two cities: The genetic mechanisms governing calvarial bone development.Genesis (New York, N.Y. : 2000) · 2019Review
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
The calvaria (upper part of the skull) is made of plates of bone and fibrous joints (sutures and fontanelles), and the proper balance and organization of these components are crucial to normal development of the calvaria. In a mouse embryo, the calvaria develops from a layer of head mesenchyme that surrounds the brain from shortly after mid-gestation. The mesenchyme just above the eye (supra-orbital mesenchyme, SOM) generates ossification centers for the bones, which then grow toward the apex gradually. In contrast, the mesenchyme apical to SOM (early migrating mesenchyme, EMM), including the area at the vertex, does not generate an ossification center. As a result, the dorsal midline of the head is occupied by sutures and fontanelles at birth. To date, the molecular basis for this regional difference in developmental programs is unknown. The current study provides vital insights into the genetic regulation of calvarial patterning. First, we showed that osteogenic signals were active in both EMM and SOM during normal development, which suggested the presence of an anti-osteogenic factor in EMM to counter the effect of these signals. Subsequently, we identified Lmx1b as an anti-osteogenic gene that was expressed in EMM but not in SOM. Furthermore, head mesenchyme-specific deletion of Lmx1b resulted in heterotopic ossification from EMM at the vertex, and craniosynostosis affecting multiple sutures. Conversely, forced expression of Lmx1b in SOM was sufficient to inhibit osteogenic specification. Therefore, we conclude that Lmx1b plays a key role as an anti-osteogenic factor in patterning the head mesenchyme into areas with different osteogenic competence. In turn, this patterning event is crucial to generating the proper organization of the bones and soft tissue joints of the calvaria.
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