PUBLICATION
Fgf-dependent depletion of microRNA-133 promotes appendage regeneration in zebrafish
- Authors
- Yin, V.P., Thomson, J.M., Thummel, R., Hyde, D.R., Hammond, S.M., and Poss, K.D.
- ID
- ZDB-PUB-080326-28
- Date
- 2008
- Source
- Genes & Development 22(6): 728-733 (Journal)
- Registered Authors
- Hyde, David R., Poss, Kenneth D., Thummel, Ryan, Yin, Voot
- Keywords
- Zebrafish, fin, regeneration, miR-133, Fgf, Mps1
- MeSH Terms
-
- Animals
- Blotting, Northern
- Cell Proliferation
- Embryo, Nonmammalian/cytology
- Embryo, Nonmammalian/physiology
- Extremities/physiology*
- Fibroblast Growth Factors/metabolism*
- Fluorescent Antibody Technique
- Gene Expression Regulation, Developmental*
- MicroRNAs/physiology*
- Protein Serine-Threonine Kinases/metabolism
- Protein-Tyrosine Kinases/metabolism
- RNA, Messenger/genetics
- RNA, Messenger/metabolism
- Receptors, Fibroblast Growth Factor/metabolism
- Regeneration/physiology*
- Reverse Transcriptase Polymerase Chain Reaction
- Zebrafish/physiology*
- Zebrafish Proteins/metabolism
- PubMed
- 18347091 Full text @ Genes & Dev.
Citation
Yin, V.P., Thomson, J.M., Thummel, R., Hyde, D.R., Hammond, S.M., and Poss, K.D. (2008) Fgf-dependent depletion of microRNA-133 promotes appendage regeneration in zebrafish. Genes & Development. 22(6):728-733.
Abstract
Appendage regeneration is defined by rapid changes in gene expression that achieve dramatic developmental effects, suggesting involvement of microRNAs (miRNAs). Here, we find dynamic regulation of many miRNAs during zebrafish fin regeneration. In particular, miR-133 levels are high in uninjured fins but low during regeneration. When regeneration was blocked by Fibroblast growth factor (Fgf) receptor inhibition, high miR-133 levels were quickly restored. Experimentally increasing amounts of miR-133 attenuated fin regeneration. Conversely, miR-133 antagonism during Fgf receptor inhibition accelerated regeneration through increased proliferation within the regeneration blastema. The Mps1 kinase, an established positive regulator of blastemal proliferation, is an in vivo target of miR-133. Our findings identify miRNA depletion as a new regulatory mechaneneration through increased proliferation within the regeneration blastema. The Mps1 kinase, an established positive regulator of blastemal prolifeism for complex tissue regeneration.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping