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.
Highlights
Cellular motility and cohesion are essential processes in vertebrate early embryonic development
The three RAB5 genes in humans were used as query sequence to identify zebrafish Ensembl predictions
Their role in vesicle trafficking and endocytosis within the cell is well characterised (Gorvel et al, 1991; Bucci et al, 1992) and, for this reason, the Rab5 family has been used to understand signalling in the developing embryo (Scholpp and Brand, 2004; Hagemann et al, 2009)
Summary
Cellular motility and cohesion are essential processes in vertebrate early embryonic development. Integral to the processes are intracellular trafficking events, which direct the signalling between cells and the movement and adhesion of cells. Activation and disruption of Rab proteins have been used to understand cell movements during gastrulation and how signalling factors move though a developing embryo (Scholpp and Brand, 2004; Ulrich et al, 2005; Hagemann et al, 2009; Tay et al, 2010; Torres and Stupack, 2011). Rab proteins have been used to understand human diseases such as Alzheimer's disease (Ginsberg et al, 2010) and the motility and invasiveness of tumour cells (Torres and Stupack, 2011)
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