FIGURE

Fig. 6

ID

ZDB-FIG-101118-32

Publication

Song et al., 2010 - Neural and Synaptic Defects in slytherin, a Zebrafish Model for Human Congenital Disorders of Glycosylation

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Fig. 6

A. AAL staining is reduced in srn, gmds morphants and gmds morphants overexpressing NICD, but not in WT embryos or WT embryos overexpressing NICD. B. WT and WT overexpressing NICD had normal Zn5+ cell patterning. srn and gmds MO showed Zn5+ cell patterning defects which was rescued by NICD overexpression in gmds morphants. C. WT and WT overexpressing NICD had normal GFAP+ glia cells in spinal cord. srn and gmds morphants had reduced GFAP+ glia cells, rescued by NICD overexpression in gmds morphants (>10 embryos in each experiment). Scale bar = 40 μm. D–E. Quantification of Zn5+ cell patterning defects. There are 3–5 Zn5+ cells every 20 μm in WT, WT overexpressing NICD and gmds MO overexpressing NICD; compared to 1–8 in srn and gmds MO embryos. D, data from a representative embryo; E, distribution of all embryos (4–6 embryos; Kolmogorov-Smirnov test, * p<0.05).

Expression Data

Antibody:	zn-5
Fish:	gmds^{p31erb/p31erb} WT + MO2-gmds kca3Tg; kca4Tg kca3Tg; kca4Tg + MO2-gmds
Knockdown Reagent:	MO2-gmds
Anatomical Term:	secondary motor neuron
Stage:	Protruding-mouth

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	gmds^{p31erb/p31erb} WT + MO2-gmds kca3Tg; kca4Tg kca3Tg; kca4Tg + MO2-gmds
Knockdown Reagent:	MO2-gmds
Observed In:	axon guidance secondary motor neuron secondary motor neuron axon spinal cord glial cell
Stage:	Protruding-mouth

Phenotype Detail

Acknowledgments

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