PUBLICATION
Fgfs control homeostatic regeneration in adult zebrafish fins
- Authors
- Wills, A.A., Kidd Iii, A.R., Lepilina, A., and Poss, K.D.
- ID
- ZDB-PUB-080826-13
- Date
- 2008
- Source
- Development (Cambridge, England) 135(18): 3063-3078 (Journal)
- Registered Authors
- Lepilina, Alexandra, Poss, Kenneth D., Wills, Airon
- Keywords
- Blastema, Fgf, Fin, Homeostasis, Regeneration, Zebrafish
- MeSH Terms
-
- Amputation, Surgical
- Animals
- Animals, Genetically Modified
- Extremities/physiology*
- Fibroblast Growth Factors/genetics
- Fibroblast Growth Factors/physiology*
- Homeostasis*
- In Situ Hybridization
- Models, Biological
- Receptors, Fibroblast Growth Factor/genetics
- Regeneration/genetics
- Regeneration/physiology*
- Signal Transduction/genetics
- Signal Transduction/physiology
- Zebrafish
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 18701543 Full text @ Development
Citation
Wills, A.A., Kidd Iii, A.R., Lepilina, A., and Poss, K.D. (2008) Fgfs control homeostatic regeneration in adult zebrafish fins. Development (Cambridge, England). 135(18):3063-3078.
Abstract
Adult teleost fish and urodele amphibians possess a spectacular ability to regenerate amputated appendages, based on formation and maintenance of progenitor tissue called a blastema. Although injury-induced, or facultative, appendage regeneration has been studied extensively, the extent to which homeostatic regeneration maintains these structures has not been examined. Here, we found that transgenic inhibition of Fgf receptors in uninjured zebrafish caused severe atrophy of all fin types within 2 months, revealing a requirement for Fgfs to preserve dermal bone, joint structures and supporting tissues. Appendage maintenance involved low-level expression of markers of blastema-based regeneration, focused in distal structures displaying recurrent cell death and proliferation. Conditional mutations in the ligand Fgf20a and the kinase Mps1, factors crucial for regeneration of amputated fins, also caused rapid, progressive loss of fin structures in otherwise uninjured animals. Our experiments reveal that the facultative machinery that regenerates amputated teleost fins also has a surprisingly vigorous role in homeostatic regeneration.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping