Figure S4. Zebrafish ETO2 is required for HSC emergence, related to Figures 1-4. The zebrafish studies provide an independent confirmation of the phenotype observed in Xenopus. Figure S4, related to Figures 1-4. Zebrafish ETO2 is required for HSC emergence (A-C) As in Xenopus, Eto2 is expressed in the trunk somites (A) but not in the dorsal aorta (DA), as seen in transverse sections along the trunk (B, C), at 24hpf (hours post-fertilisation); s, somites; ICM, intermediate cell mass. (D) To test the function of ETO2 in hematopoietic development, we knocked- down its expression using a morpholino that targets the zebrafish Eto2 (Meier et al. 2006). A dose- dependent loss of the HSC markers runx1 and cmyb (another HSC marker (Murayama et al. 2006)) in the DA (black arrowheads) was observed with increasing amounts of Eto2 MO, at 28hpf. In contrast, expression of the arterial marker notch1b was unaffected. (E) At 28hpf, none of the arterial markers analysed (dll4, dlC, notch3/5; DA, black and white arrowheads (Lawson and Weinstein 2002; Nicoli et al. 2008; Rowlinson and Gering 2010)) was affected in Eto2 morphants, whereas runx1 expression was severely downregulated (red arrowheads). Flk1 expression is grossly normal in Eto2 morphants confirming normal endothelialisation. Therefore, down-regulation of Eto2 in zebrafish embryos leads to non cell-autonomous phenotypic defects that are very similar to those observed in Xenopus Eto2 morphant embryos.
Image published in: Leung A et al. (2013)
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