Fgf and Sdf-1 pathways interact during zebrafish fin regeneration
- Bouzaffour, M., Dufourcq, P., Lecaudey, V., Haas, P., and Vriz, S.
- PLoS One 4(6): e5824 (Journal)
- Registered Authors
- Dufourcq, Pascale, Haas, Petra, Lecaudey, Virginie, Vriz, Sophie
- Fibroblast growth factor, Fishes, Zebrafish, In situ hybridization, Gene expression, Epidermis, Wnt signaling cascade, Chemokines
- MeSH Terms
- Cell Differentiation
- Chemokine CXCL12/metabolism*
- Fibroblast Growth Factors/metabolism*
- Gene Expression Regulation*
- Models, Biological
- Receptors, CXCR/metabolism
- Signal Transduction
- Zebrafish Proteins/metabolism
- 19503807 Full text @ PLoS One
Bouzaffour, M., Dufourcq, P., Lecaudey, V., Haas, P., and Vriz, S. (2009) Fgf and Sdf-1 pathways interact during zebrafish fin regeneration. PLoS One. 4(6):e5824.
The chemokine stromal cell-derived factor-1 (SDF1) was originally identified as a pre-B cell stimulatory factor but has been recently implicated in several other key steps in differentiation and morphogenesis. In addition, SDF1 as well as FGF signalling pathways have recently been shown to be involved in the control of epimorphic regeneration. In this report, we address the question of a possible interaction between the two signalling pathways during adult fin regeneration in zebrafish. Using a combination of pharmaceutical and genetic tools, we show that during epimorphic regeneration, expression of sdf1, as well as of its cognate receptors, cxcr4a, cxcr4b and cxcr7 are controlled by FGF signalling. We further show that, Sdf1a negatively regulates the expression of fgf20a. Together, these results lead us to propose that: 1) the function of Fgf in blastema formation is, at least in part, relayed by the chemokine Sdf1a, and that 2) Sdf1 exerts negative feedback on the Fgf pathway, which contributes to a transient expression of Fgf20a downstream genes at the beginning of regeneration. However this feedback control can be bypassed since the Sdf1 null mutants regenerate their fin, though slower. Very few mutants for the regeneration process were isolated so far, illustrating the difficulty in identifying genes that are indispensable for regeneration. This observation supports the idea that the regeneration process involves a delicate balance between multiple pathways.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes