Roles for Fgf signaling during zebrafish fin regeneration

Kenneth D. Poss, Jiaxiang Shen, Alex Nechiporuk, Gerald McMahon, Bernard Thisse, Christine Thisse, Mark T. Keating

Research output: Contribution to journalArticlepeer-review

272 Scopus citations


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. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)347-358
Number of pages12
JournalDevelopmental Biology
Issue number2
StatePublished - Jun 15 2000
Externally publishedYes


  • Blastema
  • Fibroblast growth factors
  • Msx
  • Regeneration
  • Sonic hedgehog
  • Zebrafish

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology


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