PUBLICATION
Zebrafish Rab5 Proteins and a role for Rab5ab in nodal signalling
- Authors
- Kenyon, E.J., Campos, I., Bull, J.C., Williams, P.H., Stemple, D.L., Clark, M.D.
- ID
- ZDB-PUB-141206-3
- Date
- 2015
- Source
- Developmental Biology 397(2): 212-24 (Journal)
- Registered Authors
- Clark, Matthew D., Kenyon, Emma, Stemple, Derek L.
- Keywords
- Nodal, Rab5, Zebrafish
- MeSH Terms
-
- Animals
- Gene Knockdown Techniques
- In Situ Hybridization
- Microscopy, Electron
- Morpholinos/genetics
- Nodal Signaling Ligands/metabolism*
- Organizers, Embryonic/embryology*
- Reverse Transcriptase Polymerase Chain Reaction
- Signal Transduction/physiology*
- Zebrafish/embryology*
- Zebrafish/genetics*
- Zebrafish/metabolism
- rab5 GTP-Binding Proteins/genetics
- rab5 GTP-Binding Proteins/metabolism*
- PubMed
- 25478908 Full text @ Dev. Biol.
Citation
Kenyon, E.J., Campos, I., Bull, J.C., Williams, P.H., Stemple, D.L., Clark, M.D. (2015) Zebrafish Rab5 Proteins and a role for Rab5ab in nodal signalling. Developmental Biology. 397(2):212-24.
Abstract
The RAB5 gene family is the best characterised of all human RAB families and is essential for in vitro homotypic fusion of early endosomes. In recent years, the disruption or activation of Rab5 family proteins has been used as a tool to understand growth factor signal transduction in whole animal systems such as Drosophila melanogaster and zebrafish. In this study we have examined the functions for four rab5 genes in zebrafish. Disruption of rab5ab expression by antisense morpholino oligonucleotide (MO) knockdown abolishes nodal signalling in early zebrafish embryos, whereas overexpression of rab5ab mRNA leads to ectopic expression of markers that are normally downstream of nodal signalling. By contrast MO disruption of other zebrafish rab5 genes shows little or no effect on expression of markers of dorsal organiser development. We conclude that rab5ab is essential for nodal signalling and organizer specification in the developing zebrafish embryo.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping