<i>fgf20</i> Is Essential for Initiating Zebrafish Fin Regeneration

TLDR

Epimorphic regeneration depends on pluripotent cells that form a blastema, and in zebrafish fin regeneration Fgf20a is expressed at the epithelial‑mesenchymal boundary during initiation and later overlaps with the blastema marker msxb. We studied the dob mutant, which fails to regenerate fins due to a null fgf20a Y148S mutation that prevents blastema formation and causes abnormal regeneration epithelium. The fgf20a null mutation does not affect embryonic survival but is essential for initiating fin regeneration and controlling blastema formation.

Abstract

Epimorphic regeneration requires the presence or creation of pluripotent cells capable of reproducing lost organs. Zebrafish fin regeneration is mediated by the creation of blastema cells. Here, we characterize the devoid of blastema (dob) mutant that fails fin regeneration during initial steps, forms abnormal regeneration epithelium, and does not form blastema. This mutation has no impact on embryonic survival. Dob results from an fgf20a null mutation, Y148S. Fgf20a is expressed during initiation of fin regeneration at the epithelial-mesenchymal boundary and later overlaps with the blastema marker msxb. Thus, fgf20a has a regeneration-specific requirement, initiating fin regeneration, and controlling blastema formation.