Roles for Fgf signaling during zebrafish fin regeneration.

Published

Journal Article

Following amputation of a urodele limb or teleost fin, the formation of a blastema is a crucial step in facilitating subsequent regeneration. Using the zebrafish caudal fin regeneration model, we have examined the hypothesis that fibroblast growth factors (Fgfs) initiate blastema formation from fin mesenchyme. We find that fibroblast growth factor receptor 1 (fgfr1) is expressed in mesenchymal cells underlying the wound epidermis during blastema formation and in distal blastemal tissue during regenerative outgrowth. fgfr1 transcripts colocalize with those of msxb and msxc, putative markers for undifferentiated, proliferating cells. A zebrafish Fgf member, designated wfgf, is expressed in the regeneration epidermis during outgrowth. Furthermore, we show that a specific inhibitor of Fgfr1 applied immediately following fin amputation blocks blastema formation, without obvious effects on wound healing. This inhibitor blocks the proliferation of blastemal cells and the onset of msx gene transcription. Inhibition of Fgf signaling during ongoing fin regeneration prevents further outgrowth while downregulating the established expression of blastemal msx genes and epidermal sonic hedgehog. Our findings indicate that zebrafish fin blastema formation and regenerative outgrowth require Fgf signaling.

Full Text

Duke Authors

Cited Authors

  • Poss, KD; Shen, J; Nechiporuk, A; McMahon, G; Thisse, B; Thisse, C; Keating, MT

Published Date

  • June 2000

Published In

Volume / Issue

  • 222 / 2

Start / End Page

  • 347 - 358

PubMed ID

  • 10837124

Pubmed Central ID

  • 10837124

Electronic International Standard Serial Number (EISSN)

  • 1095-564X

International Standard Serial Number (ISSN)

  • 0012-1606

Digital Object Identifier (DOI)

  • 10.1006/dbio.2000.9722

Language

  • eng