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Fig. 2

ID
ZDB-IMAGE-161219-34
Source
Figures for Pillay et al., 2016
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Figure Caption

Fig. 2

RA-deficient embryos exhibit relatively normal gross embryonic vasculogenesis.

(A, A') Lateral view of live 48 hpf Tg(gata1:DsRed)sd2Tg embryos with anterior to the left. Compared to wild type (WT) embryos (A), aldh1a2-morphants (A') display visible circulating blood cells, and an intact dorsal aorta and posterior cardinal vein. (B-C') Representative embryos following in situ hybridization analysis of kdrl vasculature marker gene expression (B, B') or efnb2a arterial marker gene expression (C, C') in 28 hpf embryos. Lateral view of gene expression in the dorsal aorta region of the trunk is shown in flat-mount embryos, with anterior to the left. Compared to WT embryos (B), aldh1a2-morphants (B') exhibit normal dorsal aorta kdrl gene expression. Compared to DMSO-treated controls (C), embryos treated with 5 μM DEAB (C') exhibit normal levels, but a reduced domain of dorsal aorta efnb2a gene expression. (D) Graph demonstrating the mean proportion of WT or aldh1a2-morphant embryos with intact circulation at 28 hpf and 48 hpf. Error bars represent standard error. *Indicates statistically significant difference compared to WT (P = 0.0196). See text for statistical tests. (E-G) Lateral view of dorsal aorta region of the trunk is shown in representative flat-mount Tg(kdrl:GFP)la116Tg 28 hpf embryos, with anterior to the left. Brackets indicate dorsal aorta. Compared to DMSO-treated controls (E), 2.5 μM DEAB-treated embryos (F) exhibit normal dorsal aorta morphology, while 5 μM DEAB-treated embryos (G) exhibit thinning of the dorsal aorta.

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