PUBLICATION
Zebrafish Mir Antagonizes Frizzled 7-Induced Gastrulation Defects
- Authors
- Knowlton, M.N. and Kelly, G.M.
- ID
- ZDB-PUB-050628-2
- Date
- 2004
- Source
- Zebrafish 1(2): 133-144 (Journal)
- Registered Authors
- Kelly, Greg, Knowlton, Michelle
- Keywords
- none
- MeSH Terms
- none
- PubMed
- 18248225 Full text @ Zebrafish
Citation
Knowlton, M.N. and Kelly, G.M. (2004) Zebrafish Mir Antagonizes Frizzled 7-Induced Gastrulation Defects. Zebrafish. 1(2):133-144.
Abstract
Although Xenopus studies have shown that Frizzled 7 activates at least two noncanonical signaling pathways, it is less clear which, if any, of these signaling pathways are downstream of Frizzled 7 in zebrafish. Cotransfection of Frizzled 7a (Fz7a) or Frizzled 7 (Fz7) and Xenopus Dsh-GFP results in the translocation of Dsh from the cytoplasm to the plasma membrane, a key step in canonical and noncanonical Wnt signaling. Overexpression of both zebrafish Frizzled 7 orthologs perturbs gastrulation, leading to tail defects. Rescue experiments using downstream components of the Xenopus noncanonical Wnt pathways indicate that zebrafish Fz7a and Fz7 signal through different noncanonical components. Although co-injection of pertussis toxin or a dominant negative Cdc42 rescues incomplete gastrulation caused by Fz7a, neither has any significant effect on Fz7 induced gastrulation defects. Likewise, the Fz7 overexpression phenotype, but not that of Fz7a, is rescued by myosin regulatory light chain interacting protein (Mir) and its binding partner Annexin V. Together these results indicate that Fz7a and Fz7 signal through different pathways during zebrafish gastrulation, and that Mir and Annexin V antagonize Fz7 signaling.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping