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. 2012 Jul 15;139(14):2614–2624. doi: 10.1242/dev.076018

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Fig. 8. — Six3 represses wnt8b expression in a Foxg1a-independent manner. (A-D) Expression of axin2 (A,B) and wnt8b (C,D) in control (A,C) and six3b;six7-deficient embryos (B,D) at the 8-somite stage. Black arrowhead indicates anterior limit of expression. (E-H) wnt8b (purple) and six3b (red) expression in UIC embryos (E), UIC Tg(hsp70l:Gal4-VP16); Tg(UAS:six3b) embryos misexpressing six3b (F), MO2-foxg1a-injected embryos (G) and MO2-foxg1a-injected Tg(hsp70l:Gal4-VP16); Tg(UAS:six3b) embryos misexpressing six3b (H) at 24 hpf. Embryos are shown in lateral view with anterior towards the left. Red and green arrowheads indicate dorsal and ventral edges of the telencephalon, respectively. Scale bars: 100 μm. (I) Genetic model of Six3 function in zebrafish telencephalon DV patterning. Six3 and Hh signaling function in parallel to promote foxg1a expression, which in turn promotes ventral telencephalon. Six3 and Foxg1a each can repress expression of Wnt/β-catenin ligands such as wnt8b, which can repress ventral telencephalon.