PUBLICATION
Amyloid precursor protein is required for convergent-extension movements during Zebrafish development
- Authors
- Joshi, P., Liang, J.O., Dimonte, K., Sullivan, J., and Pimplikar, S.W.
- ID
- ZDB-PUB-090814-7
- Date
- 2009
- Source
- Developmental Biology 335(1): 1-11 (Journal)
- Registered Authors
- Liang, Jennifer
- Keywords
- amyloid precursor protein, zebrafish, function, embryonic development, gastrulation, convergent extension, APPswe
- MeSH Terms
-
- Alzheimer Disease/genetics
- Alzheimer Disease/physiopathology
- Amyloid beta-Protein Precursor/classification
- Amyloid beta-Protein Precursor/genetics
- Amyloid beta-Protein Precursor/metabolism*
- Animals
- Gene Expression Regulation, Developmental*
- Gene Knockdown Techniques
- Humans
- In Situ Hybridization
- Mice
- Mutation
- Oligonucleotides, Antisense/genetics
- Oligonucleotides, Antisense/metabolism
- Phenotype
- Phylogeny
- Zebrafish/anatomy & histology
- Zebrafish/embryology*
- Zebrafish/physiology
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 19664615 Full text @ Dev. Biol.
Citation
Joshi, P., Liang, J.O., Dimonte, K., Sullivan, J., and Pimplikar, S.W. (2009) Amyloid precursor protein is required for convergent-extension movements during Zebrafish development. Developmental Biology. 335(1):1-11.
Abstract
Amyloid precursor protein (APP) has been a focus of intense investigation because of its role in Alzheimer's disease (AD), however, its biological function remains uncertain. Loss of APP and APP-like proteins results in postnatal lethality in mice, suggesting a role during embryogenesis. Here we show that in a zebrafish model system, knock down of APP results in the generation of fish with dramatically reduced body length and a short, curly tail. In situ examination of gene expression suggests that the APP morphant embryos have defective convergent-extension movements. We also show that wild-type human APP rescues the morphant phenotype, but the Swedish mutant APP, which causes familial AD (fAD), does not rescue the developmental defects. Collectively, this work demonstrates that the zebrafish model is a powerful system to define the role of APP during embryonic development and to evaluate the functional activity of fAD mutant APP.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping