Scott Stewart

This study uses zebrafish fras1 mutants to investigate Fraser Syndrome's role in fin skeletal patterning, revealing defects in basal epidermis and osteoblast integration during development and regeneration.

The paper identifies IGFR/mTOR signaling as a driver of increased translation during zebrafish fin regeneration, accelerating outgrowth through coordinated cell behavior.

The paper investigates how Shh signaling and basal epidermal collective migration drive skeletal branching in zebrafish fins during development.

The paper shows that the longfint2 mutation causes overexpression of kcnh2a, leading to prolonged fin outgrowth through ion signaling in the mesenchymal lineage.

This study shows that Ezh2-driven PRC2 activity is critical for early zebrafish embryogenesis, particularly in craniofacial development and axial skeleton patterning, with limited redundancy from Ezh1.