Related Experiment Video
Updated: Jun 22, 2026

07:22
In vivo Electroporation of Morpholinos into the Regenerating Adult Zebrafish Tail Fin
Published on: March 29, 2012
Fgf and Sdf-1 pathways interact during zebrafish fin regeneration
Mohamed Bouzaffour1, Pascale Dufourcq, Virginie Lecaudey
1Université Paris Diderot, Paris, France.
Plos One
|June 9, 2009
Summary
Fibroblast Growth Factor (FGF) signaling controls the expression of stromal cell-derived factor-1 (SDF1) during zebrafish fin regeneration. SDF1 then negatively regulates FGF signaling, revealing a feedback loop crucial for this complex regenerative process.
Area of Science:
- Developmental Biology
- Regenerative Medicine
- Molecular Signaling
Background:
- Stromal cell-derived factor-1 (SDF1) and Fibroblast Growth Factor (FGF) signaling pathways are implicated in differentiation, morphogenesis, and epimorphic regeneration.
- Understanding the interplay between these pathways is crucial for elucidating the mechanisms of tissue repair.
Purpose of the Study:
- To investigate the interaction between FGF and SDF1 signaling pathways during adult zebrafish fin regeneration.
- To determine the role of SDF1 and its receptors in FGF-mediated regeneration.
Main Methods:
- Utilized pharmaceutical and genetic tools in zebrafish models.
- Analyzed the expression of sdf1 and its receptors (cxcr4a, cxcr4b, cxcr7) under FGF signaling control.
- Investigated the regulatory relationship between Sdf1a and fgf20a expression.
Main Results:
- FGF signaling controls the expression of sdf1 and its cognate receptors during epimorphic regeneration.
- Sdf1a negatively regulates fgf20a expression, indicating a feedback mechanism.
- SDF1 signaling partially relays FGF function in blastema formation.
- SDF1-null mutants regenerate fins, albeit at a slower rate, suggesting pathway redundancy.
Conclusions:
- FGF signaling's role in blastema formation is partly mediated by SDF1.
- SDF1 provides negative feedback on the FGF pathway, transiently regulating Fgf20a expression.
- Zebrafish fin regeneration involves a complex balance of multiple signaling pathways, not solely dependent on SDF1.

