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. 2009 Dec 4;106(52):22305–22310. doi: 10.1073/pnas.0901932106

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Fig. 4. — MO knockdown of nf1a results in vascular patterning defects at 48 and 72 hpf. (A–C) At 48 hpf, nf1a ATG MO-treated Tg(fli:egfp)y1 (endothelial-specific GFP transgenic) zebrafish embryos display gross defects in vascular development compared with control MO-treated or uninjected samples. Morphant embryos (C) display abnormal claw-like projections at the leading edge of the developing intersomitic vessels and fail to develop the dorsal longitudinal anastomotic vessel (DLAV) present in both control MO-treated (B) and uninjected (A) samples. (D–F) At 72 hpf, nf1a ATG morphant embryos display only rudimentary DLAVs and a general disorganization of the trunk vasculature (F) when compared with control MO-treated (E) or uninjected (D) embryos. (Scale bars: 25 μm.)