Simplet controls cell proliferation and gene transcription during zebrafish caudal fin regeneration
- Kizil, C., Otto, G.W., Geisler, R., Nüsslein-Volhard, C., and Antos, C.L.
- Developmental Biology 325(2): 329-340 (Journal)
- Registered Authors
- Antos, Christopher, Geisler, Robert, Kizil, Caghan, Nüsslein-Volhard, Christiane, Otto, Georg
- Zebrafish, Fin regeneration, simplet, fam53b, Cell proliferation, Antisense morpholino-mediated knock down
- MeSH Terms
- Animals, Genetically Modified
- Cell Proliferation*
- Epidermis/growth & development
- Extremities/growth & development
- Gene Expression Regulation
- Mesoderm/growth & development
- Transcription Factors/genetics
- Transcription Factors/physiology*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/physiology*
- 19014929 Full text @ Dev. Biol.
Kizil, C., Otto, G.W., Geisler, R., Nüsslein-Volhard, C., and Antos, C.L. (2009) Simplet controls cell proliferation and gene transcription during zebrafish caudal fin regeneration. Developmental Biology. 325(2):329-340.
Two hallmarks of vertebrate epimorphic regeneration are a significant increase in the proliferation of normally quiescent cells and a re-activation of genes that are active during embryonic development. It is unclear what the molecular determinants are that regulate these events and how they are coordinated. Zebrafish have the ability to regenerate several compound structures by regulating cell proliferation and gene transcription. We report that fam53b/simplet (smp) regulates both cell proliferation and the transcription of specific genes. In situ hybridization and quantitative RT-PCR experiments showed that amputation of zebrafish hearts and fins resulted in strong up-regulation of the smp gene. In regenerating adult fin, smp expression remained strong in the distal mesenchyme which later expanded to the basal layers of the distal epidermis and distal tip epithelium. Morpholino knockdown of smp reduced regenerative outgrowth by decreasing cell proliferation as measured by BrdU incorporation and histone H3 phosphorylation. In addition, smp knockdown increased the expression of msxb, msxc, and shh, as well as the later formation of ectopic bone. Taken together, these data indicate a requirement for smp in fin regeneration through control of cell proliferation, the regulation of specific genes and proper bone patterning.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes