Gabriel A. Yette

This study identifies fibrillin 3 as a target of Shh/Smo signaling in zebrafish fin regeneration, showing its role in ray branching through microfibril dynamics and cell interactions.

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.

The paper shows that zebrafish fin regeneration size and shape depend on niche cells and skeletal geometry, not cell memories.