Fig. S7
- ID
- ZDB-FIG-101118-41
- Publication
- Song et al., 2010 - Neural and Synaptic Defects in slytherin, a Zebrafish Model for Human Congenital Disorders of Glycosylation
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NICD overexpression suppresses the increased Mauthner neuron phenotype in gmds morphants. A. AAL staining is reduced in gmds morphants overexpressing NICD, but not in WT embryos or WT embryos overexpressing NICD. B. WT embryos have a pair of Mauthner neurons. WT overexpressing NICD showed dramatic hindbrain patterning defects, resulting in an almost complete loss of Mauthner neurons. gmds morphants overexpressing NICD showed similar reduction of Mauthner neurons. This result suggests NICD overexpression suppresses the increase of Mauthner neurons observed in gmds morphants and thus supports our conclusion that reduction of Notch-Delta signaling in srn mutants is responsible for the neurogenesis defects (3–4 embryos assessed for each manipulation). Scale bar = 20 μm. |