Runx2-Twist1 interaction coordinates cranial neural crest guidance of soft palate myogenesis.
Xia HanJifan FengTingwei GuoYong-Hwee Eddie LohYuan YuanThach-Vu HoCourtney Kyeong ChoJingyuan LiJunjun JingEva JaneckovaJinzhi HeFei PeiJing BiBrian SongXiangfei ChaiPublished in: eLife (2021)
Cranial neural crest (CNC) cells give rise to bone, cartilage, tendons, and ligaments of the vertebrate craniofacial musculoskeletal complex, as well as regulate mesoderm-derived craniofacial muscle development through cell-cell interactions. Using the mouse soft palate as a model, we performed an unbiased single-cell RNA-seq analysis to investigate the heterogeneity and lineage commitment of CNC derivatives during craniofacial muscle development. We show that Runx2, a known osteogenic regulator, is expressed in the CNC-derived perimysial and progenitor populations. Loss of Runx2 in CNC-derivatives results in reduced expression of perimysial markers (Aldh1a2 and Hic1) as well as soft palate muscle defects in Osr2-Cre;Runx2fl/fl mice. We further reveal that Runx2 maintains perimysial marker expression through suppressing Twist1, and that myogenesis is restored in Osr2-Cre;Runx2fl/fl;Twist1fl/+ mice. Collectively, our findings highlight the roles of Runx2, Twist1, and their interaction in regulating the fate of CNC-derived cells as they guide craniofacial muscle development through cell-cell interactions.
Keyphrases
- single cell
- rna seq
- transcription factor
- high throughput
- skeletal muscle
- epithelial mesenchymal transition
- induced apoptosis
- cell therapy
- poor prognosis
- stem cells
- signaling pathway
- bone marrow
- dna methylation
- bone mineral density
- gene expression
- genome wide
- binding protein
- adipose tissue
- metabolic syndrome
- oxidative stress
- postmenopausal women
- data analysis