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Fig. 6

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ZDB-IMAGE-120517-6
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Figures for Gongal et al., 2011
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Fig. 6

hmx4 deficiency causes defects in Shh signaling. The Shh target genes ptc1 (A–B) and nkx2.2a (C–D) are reduced in 18 hpf hmx4 morphants. Dorsal–ventral extents of expression are denoted by the bracket. shha expression is unaffected in the forebrain (E–F), notochord and floor plate (G–H) in hmx4 morphant embryos. (I–J) shhb expression is upregulated in the ventral floor plate of hmx4 morphants. Sections through the forebrain reveal that hmx4 morphants have a dorsal expansion of gli1 expression (K–L). gli2 expression is unchanged in morphants (M–N), while gli3 expression is strongly reduced (O–P). Sections through the forebrain reveal that pax2a is expanded throughout the forebrain of hmx4 morphants (Q–R). (S) qPCR showing the significantly reduced relative levels of gli3 transcription in hmx4 morphants, with the levels in wild type embryos set to 1 (see text for statistical tests). Error bars indicate standard deviation.

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Reprinted from Developmental Biology, 355(1), Gongal, P.A., March, L.D., Holly, V.L., Pillay, L.M., Berry-Wynne, K.M., Kagechika, H., and Waskiewicz, A.J., Hmx4 regulates Sonic hedgehog signaling through control of retinoic acid synthesis during forebrain patterning, 55-64, Copyright (2011) with permission from Elsevier. Full text @ Dev. Biol.