Fig. S1

Fig. S1 Leo1^LA1186 mutants do not have general developmental delay. (A, B) pax2 expression is detected in the midbrain–hindbrain boundary (mhb), thyroid (t), otic vesicle (ov), and pronephric ducts (pr) of wild-type embryos (A) at 50 hpf. Leo1^LA1186 mutants have normal expression of pax2 in all of these structures at 50 hpf (B), indicating that the timely organogenesis of the brain, thyroid, otic vesicle, and pronephric ducts does not require Leo1 activity. (C, D) At 50 hpf, both wild-type (C) and leo1^LA1186 mutant (D) embryos have a leftward-looped gut, liver (l), and pancreas (p) labeled by fkd2 staining, demonstrating that the morphogenesis of the gut is not developmentally delayed upon loss of Leo1 activity. (E, F) By 50 hpf, the primary intersegmental vessels have branched dorsally to form the dorsal longitudinal anastomotic vessel (arrows) in both wild-type (E) and leo1^LA1186 mutant (F) embryos, suggesting that Leo1 activity is not essential for patterning of the trunk vasculature within a normal developmental timeframe. Vessels in E and F are visualized by fluorescence microscopy of Tg(kdrl:GFP)^la116 transgenic embryos.