Innovative JAGGED1-based therapies show promise for pediatric craniofacial bone loss, potentially overcoming limitations of current treatments with more effective and accessible solutions.

Discoidin domain receptor 2 controls craniofacial morphology by acting in skeletal progenitor cells and chondrocytes to control collagen matrix organization, chondrocyte polarity, and growth.

Within populations, there is standing variation in paralog expression levels, paralog expression levels are heritable, and variation in paralog expression can modify the phenotypes associated with mutation of one of the paralogs.

The identification of the splicing code and all the required components of alternative splicing will be crucial for a comprehensive understanding of this process in the neural crest cell biology.

Identification of heterogenous cranial neural crest (CNC)-derived cell populations and their roles in guiding craniofacial muscle development through cell-cell interactions.

A novel allele of serum response factor (SRF) reveals distinct co-factor requirements in different developmental contexts, raising issues of redundancy, threshold requirements, or novel co-factor usage.

DYRK2 regulator governs the mammalian ciliogenesis to maintain proper embryogenesis via activation of the Hh signaling during development in vivo.

Mechanosensitive channels Piezo1/2 are required for osteoblast differentiation from progenitors by sensing fluid sheer stress and matrix rigidity and regulating NFATc1, YAP1 and ß-catenin activities through Ca²⁺ stimulated phosphatase calcineurin.

Sequential live imaging of abnormal skull bone fusion in zebrafish reveals a deeply conserved role of two transcription factors, Twist1 and Tcf12, in regulating stem cell activity during growth of the skull.

Multivariate genotype-phenotype mapping enables quantification of pathway and process-level effects on complex phenotypes and predicts phenotypic effects of novel mutations.