Astra L. Henner

The paper identifies voltage-gated calcium channels as regulators of zebrafish fin regeneration, showing their role in controlling outgrowth scale through Ca2+ fluxes.

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

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

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