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Intramembranous ossification is one of the two processes involved in the development of bones within an embryo. The flat bones of the face, most of the cranial bones, and the clavicles are formed via this process. During intramembranous ossification, the bones develop directly from sheets of undifferentiated mesenchymal connective tissue.
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Related Experiment Video

Updated: Aug 8, 2025

Analyzing Craniofacial Morphogenesis in Zebrafish Using 4D Confocal Microscopy

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Published on: January 30, 2014

Ectomesenchymal Six1 controls mandibular skeleton formation.

Songyuan Luo^1,2, Zhixu Liu^1,2, Qian Bian^1,3

¹Department of Oral and Craniomaxillofacial Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Frontiers in Genetics

|February 27, 2023

Summary

Six1 is crucial for mandible development. Its absence causes craniofacial deformities by disrupting osteogenic gene expression and embryonic skeletal development pathways.

Keywords:

Six1 cranial neural crest cells craniofacial development mandibular skeletal development osteogenic differentiation

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Area of Science:

Developmental Biology
Genetics
Molecular Biology

Background:

Craniofacial development involves complex interactions of transcription factors and signaling pathways.
Six1 is a key transcription factor in craniofacial development, but its precise role in mandible formation is not fully understood.

Purpose of the Study:

To elucidate the function of Six1 in mandible development.
To investigate the molecular mechanisms by which Six1 regulates mandibular skeleton formation.

Main Methods:

Utilized Six1 knockout and cranial neural crest-specific Six1 conditional knockout mouse models.
Performed in vitro knockdown studies in C3H10 T1/2 cells.
Employed RNA sequencing (RNA-seq) to analyze gene expression changes.

Main Results:

Six1 deficiency in mice led to severe craniofacial deformities, including microsomia.
Six1's role in ectomesenchyme is critical for mandible development.
Six1 knockout/knockdown resulted in abnormal osteogenic gene expression and dysregulated embryonic skeletal development genes, including direct regulation of Bmp4, Fat4, Fgf18, and Fgfr2.

Conclusions:

Six1 is essential for proper mandibular skeleton formation during mouse embryogenesis.
Six1 regulates mandible development by controlling the expression of key osteogenic and skeletal development genes.
Six1 acts by directly binding to and promoting the transcription of genes such as Bmp4, Fat4, Fgf18, and Fgfr2.